Neurology_Adams

Neurology_Adams. As a rule, epidural hematoma arises under a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part of a devastating craniocerebral injury. A typical example is that of a child who has fallen from a bicycle or swing or has suffered some other hard blow to the head and was unconscious only momentarily. A few hours later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, seizures (which may be one sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral spasticity of the limbs and Babinski signs. The heart rate is often and is bounding as a result of a rise in systolic blood pressure (Cushing effect). The


Neurology_Adams

Neurology_Adams. the hemiparesis may give way to bilateral spasticity of the limbs and Babinski signs. The heart rate is often and is bounding as a result of a rise in systolic blood pressure (Cushing effect). The pupil may dilate on the side of the hematoma. The diagnosis can be established rapidly by revealing a lens-shaped clot with a smooth inner margin with CT and MRI (Fig. 34-8). Death, which is frequent if an expanding clot is not removed surgically, comes at the end of a comatose period and is a result of respiratory arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture.


Neurology_Adams

Neurology_Adams. Treatment of epidural hematoma The surgical procedure consists of placement of burr holes in a truly emergency situation in the ED or at the bedside or, preferably a craniotomy, drainage of the hematoma, and identification and ligation of the bleeding vessel. The operative results are excellent except in cases with extended fractures and laceration of the dural venous sinuses, in which the epidural hematoma may be bilateral rather than unilateral. If coma, bilateral Babinski signs, spasticity, or decerebrate rigidity supervene before operation, it usually means that displacement of central structures and compression of the midbrain have already occurred; prognosis is then poor, but a few patients do well if surgery is not greatly delayed. Small epidural hemorrhages can be followed by serial CT scanning and will be seen to enlarge gradually for a week or two and then be absorbed. There is controversy about the benefit of removing these smaller clots in a patient who has no symptoms or


Neurology_Adams

Neurology_Adams. CT scanning and will be seen to enlarge gradually for a week or two and then be absorbed. There is controversy about the benefit of removing these smaller clots in a patient who has no symptoms or signs; with sequential clinical and imaging surveillance, can be left alone.


Neurology_Adams

Neurology_Adams. The problems created by acute and chronic subdural hematomas are so different that they must be considered separately. In acute subdural hematoma, which may be unilateral or bilateral, there may be a brief lucid interval between the blow to the head and the advent of coma. More often, the patient is comatose from the time of the injury and the coma deepens progressively. Acute subdural hematoma may be combined with epidural hemorrhage, cerebral contusion, or laceration. The clinical effects of these several lesions are difficult to distinguish and there are a few patients in whom it is impossible to state before operation whether the clot is epidural or subdural in location. Subdural clots more than a few millimeter in thickness can be accurately visualized by the CT scan in more than 90 percent of cases, but the window settings must be appropriate to avoid obscuring of the clot by adjacent bone (Fig. 34-9). A large acute clot causes a shift of midline structure as well as marked


Neurology_Adams

Neurology_Adams. 90 percent of cases, but the window settings must be appropriate to avoid obscuring of the clot by adjacent bone (Fig. 34-9). A large acute clot causes a shift of midline structure as well as marked compression of one lateral ventricle; but if there are bilateral clots, there may be no shift and the ventricles may appear symmetrically compressed.


Neurology_Adams

Neurology_Adams. Rapidly evolving subdural hematomas are usually a result of tearing of bridging veins, and symptoms are caused by compression of the adjacent brain and of deep structures. Unlike epidural arterial hemorrhage, which is steadily progressive, the rising ICP usually arrests the venous bleeding. Exceptionally, the subdural hematoma forms in the posterior fossa and gives rise to headache, vomiting, pupillary inequality, dysphagia, cranial-nerve palsies, and, rarely, stiff neck, and ataxia of the trunk and gait if the patient is well enough to be tested for these functions. Because of their apposition to bone or an axial orientation along the tentorial dura, posterior fossa clots are likely to be overlooked in CT scans.


Neurology_Adams

Neurology_Adams. In chronic subdural hematoma, the traumatic etiology is often less clear. The head injury, especially in elderly persons and in those taking anticoagulant drugs, may have been trivial and forgotten. A period of weeks then follows when headaches (not invariable), light-headedness, slowness in thinking, apathy and drowsiness, unsteady gait, and occasionally a seizure are the main symptoms. The initial impression may be that the patient has a vascular lesion or brain tumor or is suffering from drug intoxication, a depressive illness, or Alzheimer disease. Gradual expansion of the hematoma by one of several mechanisms discussed further on is believed to cause the progression of symptoms. As with acute subdural hematoma, the disturbances of mentation and consciousness (drowsiness, inattentiveness, and confusion) are more prominent than focal or lateralizing signs, and they may fluctuate. Focal signs, when present, consist of mild hemiparesis and, rarely, an aphasic disturbance. Homonymous


Neurology_Adams

Neurology_Adams. and confusion) are more prominent than focal or lateralizing signs, and they may fluctuate. Focal signs, when present, consist of mild hemiparesis and, rarely, an aphasic disturbance. Homonymous hemianopia is seldom observed, probably because the geniculocalcarine pathway is deep and not easily compressed; similarly, hemiplegia, that is, complete paralysis of one arm and leg, is usually indicative of a lesion within the cerebral hemisphere rather than a compressive lesion on its surface. Hemiparesis from subdural hematoma may sometimes be ipsilateral to the clot, the result of compression of the contralateral cerebral peduncle against the free edge of the tentorium (Kernohan-Woltman sign; see “Pathoanatomy of Brain Displacement and Herniations” in Chap. 16). If the condition progresses, the patient becomes stuporous or comatose. But this course is often interrupted by striking fluctuations of awareness.


Neurology_Adams

Neurology_Adams. With both large acute and chronic hematomas, dilatation of the ipsilateral pupil is a fairly reliable indicator of the side of the hematoma, although this sign may be misleading, occurring on the opposite side in 10 percent of cases, according to Pevehouse and coworkers. Convulsions are seen occasionally, most often in alcoholics or in patients with cerebral contusions, but they cannot be regarded as a cardinal sign of subdural hematoma. Rare cases of internuclear ophthalmoplegia and of chorea have been reported but have not occurred in our material. Presumably they are a result of distortion of deep structures. Also, brief and self-limited disturbances of neurologic function simulating transient ischemic attacks (TIAs) may occur with chronic hematomas; their mechanism is uncertain, but they do not appear to represent seizures. In infants and children, enlargement of the head, vomiting, and convulsions are prominent manifestations of subdural hematoma.


Neurology_Adams

Neurology_Adams. CT and MRI are the most reliable diagnostic procedures. On CT scans, the acute clot is initially hyperdense but becomes slowly isodense after a period of 1 or more weeks (Fig. 34-10). At that stage it may be difficult to detect except by the tissue shifts it causes. The fluid collection then becomes progressively hypodense (with respect to the adjacent cerebral cortex) over 2 to 6 weeks. The evolution of signal changes in the MRI is similar to the sequential imaging changes found with parenchymal hematomas. The acute clot is hypointense on T2-weighted images, reflecting the presence of deoxyhemoglobin. Over the subsequent weeks, all image sequences show it as hyperintense as a result of methemoglobin formation. Eventually the chronic clot again becomes hypointense on the T1-weighted images. With contrast infusion, both imaging procedures usually reveal the vascular and reactive border surrounding the clot. Usually, by the fourth week, sometimes later, the hematoma becomes very


Neurology_Adams

Neurology_Adams. images. With contrast infusion, both imaging procedures usually reveal the vascular and reactive border surrounding the clot. Usually, by the fourth week, sometimes later, the hematoma becomes very hypodense, giving rise to a chronic subdural hygroma that is indistinguishable from idiopathic ones that are presumably caused by a rent in the arachnoid that allows CSF to escape to the subdural compartment, as discussed further on.


Neurology_Adams

Neurology_Adams. The chronic subdural hematoma becomes gradually encysted by fibrous membranes (pseudomembranes) that grow from the dura. Some hematomas, probably those in which the initial bleeding was slight (see below), resorb spontaneously. Others expand slowly and act as space-occupying masses (Fig. 34-11). Gardner, in 1932, first postulated that the gradual enlargement of the hematoma was a result of the accession of fluid, particularly CSF, which was drawn into the hemorrhagic cyst by its increasing osmotic tension as red blood cells (RBCs) hemolyzed and protein was liberated. This hypothesis, which came to be widely accepted, is not supported by the available data. It had been demonstrated that the breakdown of RBCs contributes little, if at all, to the accumulation of fluid in the subdural space. According to the latter authors, the most important factor in the expansion of subdural fluid is a pathologic permeability of the developing capillaries in the outer pseudomembrane of the hematoma.


Neurology_Adams

Neurology_Adams. According to the latter authors, the most important factor in the expansion of subdural fluid is a pathologic permeability of the developing capillaries in the outer pseudomembrane of the hematoma. The CSF plays no discernible role in this process, contrary to the original view of Munro and Merritt. The experimental observations of Labadie and Glover suggested that the volume of the original clot is a critical factor: The larger its initial size, the more likely it will be to enlarge. An inflammatory reaction, triggered by the breakdown products of blood elements in the clot, appears to be an additional stimulus for growth as well as for neomembrane formation and its vascularization. In any event, as the hematoma enlarges, the compressive effects increase gradually.


Neurology_Adams

Neurology_Adams. Treatment of subdural hematoma In most cases of acute hematoma it is sufficient to place burr holes and evacuate the clot before coma has developed. Treatment of larger hematomas, particularly after several hours have passed and the blood has clotted, consists of craniotomy to permit control of the bleeding and removal of the clot. As one would expect, the interval between loss of consciousness and the surgical drainage of the clot is perhaps the most important determinant of outcome in serious cases. Thin, crescentic clots can be observed and followed over several weeks and surgery undertaken only if focal signs or indications of increasing ICP arise (headache, vomiting, and bradycardia). Small subdural hematomas causing no symptoms and followed by CT scans will self-absorb, leaving only a deep yellow, sometimes calcified membrane attached to the inner dural surface. If the acute clot is too small to explain the coma or other symptoms, there is probably extensive contusion of the


Neurology_Adams

Neurology_Adams. a deep yellow, sometimes calcified membrane attached to the inner dural surface. If the acute clot is too small to explain the coma or other symptoms, there is probably extensive contusion of the cerebrum or another lesion.


Neurology_Adams

Neurology_Adams. To remove more chronic hematomas, a craniotomy must be performed and an attempt made to strip the membranes that surround the clot. This is said to diminish the likelihood of reaccumulation of fluid but it is not always successful. Other causes of operative failure are postoperative swelling of the compressed hemisphere or failure of the hemisphere to expand after removal of a large clot. The difficulty of managing these patients surgically should not be underestimated. Elderly patients may be slow to recover after removal of the chronic hematoma or may have a prolonged period of confusion. Postoperative expansion of the brain can be followed by serial CT scans and may take weeks. Small, asymptomatic chronic collections are usually left alone and followed serially by clinical and CT examination, first at several week and then longer intervals.


Neurology_Adams

Neurology_Adams. Although no longer a common practice, the administration of glucocorticoids was an alternative to surgical removal of subacute and chronic subdural hematomas in patients with minor symptoms or with contraindications to surgery. This approach, reviewed by Bender and Christoff decades ago, has not been studied systematically but has been successful in a few of our patients (of course, they may have improved independent of the steroids).


Neurology_Adams

Neurology_Adams. This is a thinly encapsulated collection of clear or slightly xanthochromic fluid in the subdural space; such collections form after an injury, as well as after meningitis (in an infant or young child). As often, subdural hygromas appear without precipitant, presumably because of a ball-valve effect of an arachnoidal tear that allows cerebrospinal fluid to collect in the space between the arachnoid and the dura; brain atrophy is conducive to this process. Occasionally a hygroma originates from a tear in an arachnoidal cyst. It may be difficult to differentiate a long-standing subdural hematoma from hygroma, and some chronic subdural hematomas are probably the result of repeated small hemorrhages that arise from the membranes of hygromas. Shrinkage of the hydrocephalic brain after ventriculoperitoneal shunting is also conducive to the formation of a subdural hematoma or hygroma, in which case drowsiness, confusion, irritability, and low-grade fever are relieved when the subdural fluid


Neurology_Adams

Neurology_Adams. shunting is also conducive to the formation of a subdural hematoma or hygroma, in which case drowsiness, confusion, irritability, and low-grade fever are relieved when the subdural fluid is aspirated or drained. Intracranial hypotension is another cause of subdural hygromas. In adults, hygromas are usually asymptomatic and do not require treatment; they only are infrequently the cause of seizures.


Neurology_Adams

Neurology_Adams. Severe closed head injury is almost universally accompanied by cortical contusions and surrounding edema. The mass effect of contusional swelling, if sufficiently large, becomes a major factor in the genesis of tissue shifts and raised ICP. The CT appearance of contusion was already described (see Figs. 34-4 and 34-5). In the first few hours after injury, the bleeding points in the contused area may appear small and innocuous. The main concern, however, is the tendency for a contused area to swell or to develop into a hematoma during the first several days after injury. This may give rise to delayed clinical deterioration, sometimes abrupt in onset and concurrent with the appearance of swelling of the damaged region on the CT scan. It has been claimed, on uncertain grounds, that the swelling in the region of an acute contusion is precipitated by excessive administration of intravenous fluids (fluid management is considered further on in this chapter). Craniotomy and decompression of


Neurology_Adams

Neurology_Adams. in the region of an acute contusion is precipitated by excessive administration of intravenous fluids (fluid management is considered further on in this chapter). Craniotomy and decompression of the swollen brain may be of benefit in selected cases with elevated ICP but it has no effect on the focal neurologic deficit.


Neurology_Adams

Neurology_Adams. One or several intracerebral hemorrhages may be apparent immediately after head injury, or hemorrhage may be infrequently delayed in its development by several days (the earlier mentioned spät apoplexie). The bleeding is in the subcortical white matter of one lobe of the brain or in deeper structures such as the basal ganglia or thalamus. The injury had nearly always been severe; blood vessels as well as cortical tissue are torn. The clinical picture of traumatic intracerebral hemorrhage is similar to that of hypertensive brain hemorrhage with deepening coma with hemiplegia, a dilating pupil, bilateral Babinski signs, and stertorous and irregular respirations. The additional mass may be manifest by an abrupt rise in blood pressure and in ICP.


Neurology_Adams

Neurology_Adams. Craniotomy with evacuation of an acute or delayed clot has given a successful result in some cases but the advisability of surgery is governed by several factors including the level of consciousness, the time from the initial injury, and the associated damage (contusions, subdural and epidural bleeding) shown by imaging studies. Application of ICP monitoring and of CT scans at intervals after the injury facilitates diagnosis. Boto and colleagues found that basal ganglia hemorrhages were prone to enlarge in the day or two after closed head injury and that those greater than 25 mL in volume were fatal in 9 of 10 cases.


Neurology_Adams

Neurology_Adams. It should be mentioned again that subarachnoid blood of some degree is very common after all degrees of head injury. A problem that sometimes arises in cases that display both contusions and subarachnoid blood is the possibility that a ruptured aneurysm was the initial event and that a resultant fall caused the contusions. In cases where the subarachnoid blood is concentrated around one of the major vessels of the circle of Willis, an angiogram is justified to exclude the latter possibility. Also in elderly patients, it has been difficult to determine whether a fall had been the cause or the result of a subarachnoid or an intracerebral hemorrhage. These subjects are addressed further in Chap. 33.


Neurology_Adams

Neurology_Adams. This condition is seen in the first hours after injury and may prove rapidly fatal. The CT scan shows enlargement of both hemispheres and compression of the basal cisterns and ventricles. There is usually no papilledema in the early stages, during which the child hyperventilates, vomits, and shows extensor posturing. The assumption has been that this represents a loss of regulation of cerebral blood flow and a massive increase in the blood volume of the brain. The administration of excessive water in intravenous fluids may contribute to the problem and should be avoided. Inappropriate secretion of antidiuretic hormone also exaggerates the swelling in some children. We have not observed this complication in adults. Fear of massive brain swelling from a second impact after a concussion has been raised as a rationale for keeping youngsters from returning to athletic activity, but there is only limited evidence for the existence of this entity in adults as noted by McCrory and Berkovic.


Neurology_Adams

Neurology_Adams. This form of craniocerebral trauma in infants is known in large emergency practices and is now missed less frequently than in the past as practitioners have been sensitized to consider it as a form of child abuse when an infant or child is injured. As the name implies, the inciting trauma is typically violent shaking of the body or head of an infant, resulting in rapid acceleration and deceleration of the cranium. The presence of this type of injury is inferred from the distribution and types of lesions on imaging studies or autopsy examination, but precision in examination is paramount because of its forensic and legal implications. The diagnosis is suspected from the combination of subdural hematomas and retinal hemorrhages, as summarized by Bonnier and colleagues. Sometimes there are occult skull fractures, but more often, there is little or no direct cranial trauma. Additional lesions may be evident on diffusion-weighted MRI, particularly in the white matter of the corpus callosum


Neurology_Adams

Neurology_Adams. skull fractures, but more often, there is little or no direct cranial trauma. Additional lesions may be evident on diffusion-weighted MRI, particularly in the white matter of the corpus callosum and the temporo-occipito-parietal region. This syndrome confers a high risk for slowing of cognitive development; in extreme cases there may be acquired microcephaly reflecting brain atrophy consequent to both contusions and infarctions. A low initial Glasgow Coma Scale score, retinal hemorrhages, and skull fractures are associated with poor outcomes. Old and recent fractures in other parts of the body should arouse suspicion of this syndrome.


Neurology_Adams

Neurology_Adams. The descriptions in the preceding pages apply to blunt, nonpenetrating injuries of the skull and their effects on the brain. In the past, the care of penetrating craniocerebral injuries was mainly the interest of the military surgeon, but—with the persistence of violent crime in society—such cases have also become commonplace on the emergency wards of general hospitals.


Neurology_Adams

Neurology_Adams. In civilian life, missile injuries are essentially caused by bullets fired from rifles or handguns at high velocities. Air is compressed in front of the bullet so that it has an explosive effect on entering tissue and causes damage for a considerable distance around the missile track. Missile fragments, or shrapnel, from exploding shells, mines, grenades, or bombs are the usual causes of penetrating cranial injuries in wartime. The cranial wounds that result from missiles and shrapnel have been classified by Purvis as tangential, with scalp lacerations, depressed skull fractures, and meningeal and cerebral lacerations; penetrating, with in-driven metal particles, hair, skin, and bone fragments; and through-and-through wounds.


Neurology_Adams

Neurology_Adams. In most penetrating injuries from high-velocity missiles, the object (such as a bullet) causes a high-temperature coagulative lesion that is sterile and does not require surgery if the projectile exits the skull. In these instances, the main considerations are the development of infection or CSF leaks or, in the long term, epilepsy or aneurysms in distal blood vessels. The latter are considered to be the result of disruption of the vessel wall by the local high-energy shock wave. If the brain is penetrated at the lower levels of the brainstem, death is instantaneous because of respiratory and cardiac arrest. Even through-and-through wounds at higher levels, as a result of energy dissipated in the brain tissue, may damage vital centers sufficiently to cause death immediately or within a few minutes.


Neurology_Adams

Neurology_Adams. Once the initial complications are dealt with, the surgical problems, as outlined by Meirowsky, are reduced to three: prevention of infection by debridement accompanied by the administration of broad-spectrum antibiotics; control of increased ICP and shift of mid-line structures by removal of clots of blood and the administration of mannitol or other dehydrating agents, and the prevention of life-threatening systemic complications.


Neurology_Adams

Neurology_Adams. When first seen, the majority of patients with penetrating cerebral lesions are comatose. A small metal fragment may have penetrated the skull without causing concussion, but this is usually not true of high-velocity missiles. In a series of 132 patients analyzed by Frazier and Ingham, consciousness was lost initially in 120. The depth and duration of coma seemed to depend on the degree of cerebral necrosis, edema, and hemorrhage. In the series of the Traumatic Coma Data Bank, the mortality rate in 163 patients who were initially comatose from a cranial gunshot wound is 88 percent—more than twice the rate from severe blunt head injury. On emerging from coma, the patient passes through states of stupor, confusion, and amnesia, not unlike those following severe closed head injuries. Focal or focal and generalized seizures occur in the early phase of the injury in some 15 to 20 percent of cases.


Neurology_Adams

Neurology_Adams. Recovery may take months. Frazier and Ingham commented on the “loss of memory, slow cerebration, indifference, mild depression, inability to concentrate, sense of fatigue, irritability, vasomotor, and cardiac instability, frequent seizures, headaches, and giddiness, all reminiscent of the residual symptoms from severe closed head injury with contusions.” Every possible combination of focal cerebral symptoms may be caused by such lesions. The excellent older articles by Feiring and Davidoff, by Russell, and by Teuber are still very useful references on this subject. Epilepsy is the most troublesome long-term sequela and is described further on. Ascroft and also Caviness, in reviewing World War II cases, found that approximately half of all patients with bullet or shrapnel wounds that had penetrated the dura eventually developed seizures, most focal in nature; the figures reported by Caveness for Korean War veterans are about the same.


Neurology_Adams

Neurology_Adams. CSF rhinorrhea, discussed earlier and in Chap. 29, may occur as an acute manifestation of a penetrating injury that produces a fracture through the frontal, ethmoid, or sphenoid bones. Cairns listed these acute cases as a separate group in his classification of CSF rhinorrheas, the others being (1) a delayed form after craniocerebral injury, (2) a form that follows sinus and cranial surgery, and (3) a spontaneous variety. Pneumoencephalocele (aerocele)—that is, air entering the cerebral subarachnoid space or ventricles spontaneously or as a result of sneezing or blowing the nose—is evidence of an opening from the paranasal sinus through the dura, as mentioned earlier in relation to skull fracture (see Fig. 34-3).


Neurology_Adams

Neurology_Adams. The shock wave of an explosive device such as bomb can propel objects into the cranium but there is also a direct form of organ damage from the dissipation of energy that occurs at the interfaces of tissues of different densities. This form of barotrauma invariably ruptures the tympanic membranes, a sign that is a marker of blast injury (Xydakis et al). Deafness, tinnitus, and vertigo are common accompaniments from cochlear concussion. The lung is next most often affected.


Neurology_Adams

Neurology_Adams. Loss of consciousness may occur but there is little understanding of the mechanism aside from the conventional configuration of flinging of the skull from the pressure wave. As summarized in an editorial by one of the authors, the initial shock wave is followed by a supersonic blast wind and a reverse and prolonged front of underpressure. Tissues are damaged when energy is dissipated at the interface between air and liquid that presents a change in acoustic impedance. The subsequent blast wind is the source of separate injury, throwing people against fixed objects and dispersing projectiles that penetrate the body. Potential modes of conduction of the force of the blast to the cranial contents include the acceleration and deceleration of the head as a wave passes by, which essentially results in concussion; skull deformation which squeezes the brain; the indirect passage of the shock wave through the lungs; and the entry of the wave through the openings in the cranial vault,


Neurology_Adams

Neurology_Adams. results in concussion; skull deformation which squeezes the brain; the indirect passage of the shock wave through the lungs; and the entry of the wave through the openings in the cranial vault, specifically the acoustic and optic canals and the foramen magnum.


Neurology_Adams

Neurology_Adams. Acute gas embolism of the brain vessels has also been reported in the military medical literature. DePalma and colleagues and also Ropper have reviewed blast injuries but the neurologic literature is quite deficient and does not settle whether the percussion wave can produce unconsciousness by direct “concussion” in the original sense of the term, causing “commotion” of brain tissue or perhaps momentary cessation of cerebral blood flow. Posttraumatic Epilepsy (See Also Chap. 15)


Neurology_Adams

Neurology_Adams. Seizures are the most common delayed sequela of craniocerebral trauma, with an overall incidence of approximately 5 percent in patients with closed head injuries and 50 percent in those who had sustained a compound skull fracture and direct wounds of the brain. The basis is nearly always a contusion or laceration of the cortex. As one might expect, the risk of developing posttraumatic epilepsy is also related to the overall severity of the closed head injury. In a civilian cohort of 2,747 head-injured patients described by Annegers and colleagues (1980), the risk of seizures after severe head injury (defined by loss of consciousness or amnesia for more than 24 h, including subdural hematoma and brain contusion) was 7 percent within 1 year and 11.5 percent in 5 years. If the injury was only moderate (unconsciousness or amnesia for 30 min to 24 h or causing only a skull fracture), the risk fell to 0.7 and 1.6 percent, respectively. After mild injury (loss of consciousness or amnesia of


Neurology_Adams

Neurology_Adams. moderate (unconsciousness or amnesia for 30 min to 24 h or causing only a skull fracture), the risk fell to 0.7 and 1.6 percent, respectively. After mild injury (loss of consciousness or amnesia of less than 30 min), the incidence of seizures was not significantly greater than in the general population. In a subsequent study, Annegers and colleagues (1998) expanded the original cohort to include 4,541 children and adults with cerebral trauma. The results were much the same as those of the first study except that in patients with mild closed head injuries, there was only a slight excess risk of developing seizures—a risk that remained elevated only until the fifth year after injury. The likelihood of epilepsy is said to be greater in parietal and posterior frontal lesions, but it may arise from lesions in any area of the cerebral cortex. Also, the frequency of seizures is considerably higher after penetrating cranial injury, as cited earlier.


Neurology_Adams

Neurology_Adams. The interval between the head injury and the first seizure varies greatly. A small number of patients have convulsive movements within moments of the injury (immediate epilepsy). Usually this amounts to a brief tonic extension of the limbs, with slight shaking movements immediately after concussion, followed by awakening in a mild confusional state. Whether this represents a true epileptic phenomenon or, as appears more likely, is the result of arrest of cerebral blood flow or a transient brainstem dysfunction is unclear. Some 4 to 5 percent of hospitalized head-injured individuals are said to have one or more seizures within the first week of their injury (early epilepsy). The immediate seizures have a good prognosis and we tend not to treat them as if they represented epilepsy; on the other hand, late seizures are significantly more frequent in patients who had experienced epilepsy in the first week after injury (not including the convulsions of the immediate injury; Jennett).


Neurology_Adams

Neurology_Adams. the other hand, late seizures are significantly more frequent in patients who had experienced epilepsy in the first week after injury (not including the convulsions of the immediate injury; Jennett). Seizures occurring minutes or hours after the injury in an otherwise fully awake patient have sometimes turned out to be factitious in our experience.


Neurology_Adams

Neurology_Adams. The term “posttraumatic epilepsy” usually refers to late epilepsy, that is, to seizures that develop several weeks or months after closed head injury (1 to 3 months in most cases). Approximately 6 months after injury, half the patients who will develop epilepsy have had their first episode; by the end of 2 years, the figure rises to 80 percent (Walker). Data derived from a 15-year study of military personnel with severe (penetrating) brain wounds indicate that patients who escape seizures for 1 year after injury can be 75 percent certain of remaining seizure free; patients without seizures for 2 years can be 90 percent certain; and for 3 years, 95 percent certain. For the less-severely injured (mainly closed head injuries), the corresponding times are 2 to 6 months, 12 to 17 months, and 21 to 25 months (Weiss et al). Despite this, there is no doubt that seizures in adulthood occur for which there is no other explanation than a small scarred cortical contusion that had been acquired


Neurology_Adams

Neurology_Adams. 21 to 25 months (Weiss et al). Despite this, there is no doubt that seizures in adulthood occur for which there is no other explanation than a small scarred cortical contusion that had been acquired decades before. The interval between head injury and development of seizures is said to be longer in children.


Neurology_Adams

Neurology_Adams. Posttraumatic seizures (both focal and generalized) tend to decrease in frequency as the years pass, and a significant number of patients (10 to 30 percent, according to Caviness) eventually stop having them. Status epilepticus is uncommon. Individuals who have early attacks (within a week of injury) are more likely to have a complete remission of their seizures than those whose attacks begin a year or so after injury. A low frequency of attacks is another favorable prognostic sign. Alcoholism is considered to have an adverse effect on this seizure state, but there are no systematic studies of this subject. Our colleague, M. Victor, observed some 25 patients with posttraumatic epilepsy in whom seizures had ceased altogether for several years, only to recur in relation to drinking. In these patients the seizures were precipitated by a weekend or even one evening of heavy drinking and occurred, as a rule, not when the patient was intoxicated but in the withdrawal period.


Neurology_Adams

Neurology_Adams. The nature of the epileptogenic lesion has been a cortical scar in most instances, but in some cases, particularly in alcoholics, it has been elusive. From the examination of old cortical contusions (plaques jaunes), one cannot, on morphologic grounds, determine whether a lesion had or had not been epileptogenic. Electrocorticograms of the brain in regions adjacent to old traumatic foci reveal a number of spontaneously electrically active zones adjacent to the scars.


Neurology_Adams

Neurology_Adams. The use of antiepileptic drugs to prevent a posttraumatic seizure and subsequent epilepsy after closed or penetrating cranial injury has its proponents, and skeptics. In one study, patients receiving phenytoin developed fewer seizures at the end of the first year than a placebo group, but a year after medication was discontinued, the incidence was the same (and quite low) in the two groups. An extensive randomized study by Temkin and colleagues demonstrated that when administered within a day of injury and continuing for 2 years, phenytoin reduced the incidence of seizures in the first week, but not thereafter. Also, in a study of a large number of patients with penetrating head injuries, the prophylactic use of antiepileptic medications was ineffective in preventing early seizures (Rish and Caveness), and this is reflected in current guidelines (Chang and Lowenstein). Subsequent studies have come to much the same conclusion.


Neurology_Adams

Neurology_Adams. Usually, persistent seizures can be controlled by a single antiepileptic medication, and relatively few seizure disorders are recalcitrant to the point of requiring excision of the epileptic focus. In this small group, the surgical results vary according to the methods of patient selection and techniques of operation. Under the neurosurgical conditions of four decades ago, with careful selection of cases, Rasmussen (also Penfield and Jasper) was able to eradicate seizures in 50 to 75 percent of cases by excision of the focus; the results currently are somewhat better.


Neurology_Adams

Neurology_Adams. A worrisome consequence of severe head injury, which is observed in some comatose patients and particularly in the vegetative state, is a syndrome of episodic vigorous extensor posturing, profuse diaphoresis, hypertension, and tachycardia lasting minutes to an hour. A slight fever may accompany the spells. Families and staff are greatly disturbed by the display, particularly when the patient’s grimacing suggests suffering. These spells of excessive sympathetic activity and posturing may be precipitated by painful stimuli or by distention of a viscus, but often they arise spontaneously. The syndrome is often mistakenly identified as a seizure and in many texts is still referred to as “diencephalic epilepsy” but it is more likely the result of the removal of suppressive cortical influences on autonomic structures, allowing the hypothalamus to function independently of normal inhibitory mechanisms. A survey of 35 such patients by Baugley and colleagues identified diffuse axonal injury


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Neurology_Adams. on autonomic structures, allowing the hypothalamus to function independently of normal inhibitory mechanisms. A survey of 35 such patients by Baugley and colleagues identified diffuse axonal injury and a period of hypoxia as being the main associated injuries and this has been our experience as well.


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Neurology_Adams. Narcotics such as morphine and benzodiazepines have a slightly beneficial effect but bromocriptine, which may be used in combination with sedatives or with small doses of morphine, has been most effective according to Rossitch and Bullard.


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Neurology_Adams. The question of a causative relationship between cerebral trauma and the development of Parkinson disease has been a controversial issue for many years—usually with the conclusion that the condition does not exist and that any apparent relationship, particularly after a single brain injury, is coincidental. Some such patients probably had early symptoms of Parkinson disease brought to light by the head injury. There are, however, cases such as the one reported by Doder and colleagues, in which traumatic necrosis of the lenticular and caudate nuclei was followed after a period of 6 weeks by the onset of predominantly contralateral parkinsonian signs, including tremor, which progressed slowly and were unresponsive to l-dopa. There are also undoubted instances of parkinsonism following severe closed head injury and the vegetative state (Matsuda et al). An exception to these statements may be a parkinsonian syndrome in ex-boxers and in others who had frequent minor head injuries, as a


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Neurology_Adams. closed head injury and the vegetative state (Matsuda et al). An exception to these statements may be a parkinsonian syndrome in ex-boxers and in others who had frequent minor head injuries, as a manifestation of the “punch-drunk” syndrome, now subsumed under the term “chronic traumatic encephalopathy.” There remains the possibility that cranial trauma incites a series of cellular events that lead to the deposition of abnormal structural proteins such as synuclein (see below).


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Neurology_Adams. Cerebellar ataxia is another rare consequence of cranial trauma, often unexplained but also in cases complicated by cerebral anoxia (causing ataxia with myoclonus) or by a hemorrhage strategically placed in the deep midbrain or cerebellum. When cerebellar ataxia is caused by the trauma itself, it is frequently unilateral and the result of injury to the superior cerebellar peduncle. We have experience with a severely ataxic patient who had only small lesions in the cerebellum after bilateral acute subdural hematomas from an assault with head trauma. An “apraxia” of gait may also reflect the presence of a communicating hydrocephalus (see below and Chap. 29).


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Neurology_Adams. Acute traumatic encephalopathy In almost all patients with cerebral concussive injury, there remains a gap in memory (traumatic amnesia) spanning a variable period from before the accident to some point following it as discussed earlier. This gap is permanent and is filled in only by what the patient is told. In addition, as stated in the introduction to this section, some degree of impairment of higher cortical function may persist for weeks (or be permanent) after moderate to severe head injuries, even after the patient has reached the stage of forming continuous memories. During the period of reduced mentation, the memory disorder is the most prominent feature; in that respect, the state resembles the alcoholic form of the Korsakoff amnesic state and has some resemblance to the state of transient global amnesia (see Chap. 20).


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Neurology_Adams. With more careful testing, other cognitive disorders are usually evident. Concussed patients, during the period of posttraumatic amnesia, rarely confabulate. Apart from disorientation in place and time, the head-injured patient also shows defects in attention, as well as showing distractibility, perseveration, and an inability to synthesize perceptual data. Judgment and executive function may be mildly impaired, rarely severely, during the amnestic epoch. A perseverative tendency interferes with both action and thought. Leininger and associates, for example, found that most of their 53 patients who suffered minor head injury in traffic accidents performed less well than controls on psychologic tests (category test, auditory verbal learning, copying of complex figures). The fact that those who were merely dazed did as poorly as those who were concussed and that litigation was involved in some cases would lead one to question these results. Perhaps most affected, and most evident to


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Neurology_Adams. who were merely dazed did as poorly as those who were concussed and that litigation was involved in some cases would lead one to question these results. Perhaps most affected, and most evident to high-functional individuals, is a problem with overall planning and coherence that is attributable to a defect in frontal lobe executive functioning.


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Neurology_Adams. As a general rule, the lower the score on the Glasgow Coma Scale immediately after injury (see Table 34-1) and the longer the posttraumatic gap in the formation of new memories (anterograde amnesia), the more likely the patient is to suffer some permanent cognitive and personality changes. According to Jennett and Bond, patients with good recovery achieved their maximum degree of improvement within 6 months. Others have found that detailed and repeated psychologic testing over a prolonged period, even in patients with relatively minor cerebral injuries, discloses measurable improvement for as long as 12 to 18 months.


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Neurology_Adams. There are other mental and behavioral abnormalities of a more subtle type that remain as sequelae to serious cerebral injury. As the stage of posttraumatic dementia recedes, the patient may find it impossible to work or to adjust to his family situation. Such patients are often abnormally abrupt, argumentative, and suspicious. Unlike the postconcussion syndrome described above, in which there is a certain uniformity, these traits vary with the patient’s age, past experience, and environmental stresses. Extremes of age have been particularly important in our experience. The most prominent behavioral abnormality in children, described by Bowman and colleagues, is a change in personality. They become impulsive, impatient, unable to sit still, or may become heedless of the consequences of their actions and lacking in appreciation of social norms—much like those who in the past had recovered from encephalitis lethargica. Some adolescents or young adults show the general lack of inhibition


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Neurology_Adams. actions and lacking in appreciation of social norms—much like those who in the past had recovered from encephalitis lethargica. Some adolescents or young adults show the general lack of inhibition and impulsivity that one associates with frontal lobe disease. In the older person, it is the impairment of intellectual functions that assumes greater prominence. In most instances, these more serious behavioral changes can be traced to contusions in the frontal and temporal lobes. In cases without obvious structural brain damage, cognitive deficiency after trauma has been widely attributed to diffuse axonal injury. Attempts to validate this by modern techniques such as diffusion tensor imaging have met with some success, such as the series described by Kraus and colleagues.


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Neurology_Adams. The tendency is for many such symptoms to subside slowly although not always completely, even in those in whom an accident has provoked a frank outburst of psychosis (as may happen to a person who is bipolar or a paranoid schizophrenic). These forms of what had colorfully in the past been called “traumatic insanity” were analyzed for the first time a century ago by the noted neuropsychiatrist, Adolf Meyer.


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Neurology_Adams. Chronic traumatic encephalopathy The cumulative effects of repeated or even single cerebral injuries, constitute a type of head injury that until recently was difficult to classify. The subject of a delayed neurodegenerative cerebral disease that follows mild traumatic brain injury after many years is best introduced by an exposition of the long-appreciated condition in boxers who had engaged in many bouts over a long period of time. This historically important syndrome serves to introduce the more recently emphasized and seemingly ubiquitous chronic encephalopathy in other professional athletes. It refers to the development after years in the ring of dysarthric speech and a state of forgetfulness, slowness in thinking, and other signs of dementia. Movements are slow, stiff, and uncertain, especially those involving the legs, and there is a shuffling, wide-based gait. In other words, a parkinsonian and dementing syndrome emerges and sometimes a moderately disabling ataxia, but there


Neurology_Adams

Neurology_Adams. especially those involving the legs, and there is a shuffling, wide-based gait. In other words, a parkinsonian and dementing syndrome emerges and sometimes a moderately disabling ataxia, but there is no mistaking these for idiopathic Parkinson or Alzheimer disease. The plantar reflexes may be extensor on one or both sides. The clinical syndrome was reanalyzed by Roberts and colleagues, who found it present to some degree in 37 of the 224 professional boxers they examined. More recent studies show that in about one-half of all professional boxers, both active and retired, the CT scan discloses ventricular dilatation and sulcal widening and a cavum septi pellucidi (why the latter, which is ostensibly a developmental anomaly, would be overrepresented in boxers is unclear). These anatomic abnormalities had been demonstrated many years before by pneumoencephalography and were found to be related to the number of bouts (Ross et al;


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Casson et al).

Neurology_Adams. Casson et al).


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Neurology_Adams. A pathologic study of this disorder specific to boxers was made by Corsellis and associates. They examined the brains of 15 retired boxers who had shown the “punch-drunk” syndrome and identified a group of cerebral changes that appeared to explain the clinical findings. Mild to moderate enlargement of the lateral ventricles and thinning of the corpus callosum were present in all cases. Also, as mentioned, practically all of them showed a greatly widened cavum septi pellucidi and fenestration of the septal leaves. Readily identified areas of glial scarring were situated on the inferior surface of the cerebellar cortex. In these areas, and well beyond them, Purkinje cells were lost and the granule cell layer was somewhat thinned. Surprisingly, cerebral cortical contusions were found in only a few cases. Notably absent also was evidence of previous hemorrhage but earlier studies by Martland emphasized punctate hemorrhages as the main finding (he may have introduced the term from the ring


Neurology_Adams

Neurology_Adams. a few cases. Notably absent also was evidence of previous hemorrhage but earlier studies by Martland emphasized punctate hemorrhages as the main finding (he may have introduced the term from the ring to medical parlance and his paper has colorful language). Of the 15 cases in Corsellis’s cohort, 11 showed varying degrees of loss of pigmented cells of the substantia nigra and locus ceruleus, and many of the remaining cells showed Alzheimer neurofibrillary change but not Lewy bodies. Neurofibrillary changes were scattered diffusely through the cerebral cortex and brainstem but were most prominent in the mediotemporal gray matter. Noteworthy was the absence of discrete amyloid plaques in this material by the usual staining methods; however, all cases showed extensive immunoreactive deposits of beta-amyloid (“diffuse plaques”).


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Neurology_Adams. However, these studies were performed before the advent of modern immunohistochemistry techniques. McKee and her coworkers have drawn attention to the deposition of tau protein in autopsy material that has come to define chronic traumatic encephalopathy. They have found a fairly consistent neuropathologic pattern consisting mainly of perivascular hyperphosphorylated tau protein embedded in astrocytic or neurofibrillary tangles with a predilection for the depths of sulci of the frontal and temporal lobes but also in other areas of cortex, thalamus, and brainstem, and eventually appearing extensively in the medial temporal lobes. For example, among 85 subjects with repetitive mild traumatic brain injury they found these changes to varying degrees in 68. The majority had headaches, depression, impulsivity, and aggression only roughly proportional to the severity of pathologic changes. As evident in others was poor cognitive performance in the spheres of executive function and memory.


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Neurology_Adams. impulsivity, and aggression only roughly proportional to the severity of pathologic changes. As evident in others was poor cognitive performance in the spheres of executive function and memory. Only those with the most widespread and densest deposition of tau were overtly demented and many of those had gait difficulty. A few of these also had parkinsonian manifestations. A putative relationship of recurrent trauma to motor neuron disease has also been raised. This form of chronic encephalopathy and tau deposition has evinced great interest in relation to concussion sustained during athletics at all levels.


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Neurology_Adams. This is an uncommon complication, but one that is frequently imputed to severe head injury. It usually conforms to the category of normal pressure hydrocephalus, as discussed in Chap. 29 but an ex-vacuo type of ventricular enlargement is seen, particularly in chronic alcoholics. Intermittent headaches, vomiting, confusion, and drowsiness are the initial manifestations. Later on, mental dullness, apathy, and psychomotor retardation are seen; by this time the CSF pressure may have fallen to a normal level (normal-pressure hydrocephalus). Postmortem examinations in some cases have demonstrated an adhesive basilar arachnoiditis. Early subarachnoid hemorrhage may be involved in the mechanisms. The response to ventriculoperitoneal shunt may be dramatic. Zander and Foroglou have written informatively about this condition.


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Neurology_Adams. This troublesome problem has been mentioned in several places earlier in the chapter, as well as in Chap. 10 in relation to headache. When the syndrome is protracted, neurologists are vexed by the condition—a problem intensified by worried patients and family. It has some similarities to the posttraumatic stress disorder, and had in the past been aptly termed “posttraumatic nervous instability syndrome” and “traumatic neurasthenia” by Sir Charles Symonds, among many other names. Headache, dizziness, poor endurance, and lack of mental clarity are the central symptoms.


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Neurology_Adams. The cranial pain is either generalized or localized to the part that had been struck and variously described as aching, throbbing, pounding, stabbing, pressing, or band like; it is remarkable for its variability in an individual patient. The intensification of the headache and other symptoms by mental and physical effort, straining, stooping, and emotional excitement is characteristic; rest and quiet tend to relieve it. Headaches may present a major obstacle to convalescence.


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Neurology_Adams. Dizziness, another prominent symptom, is usually not a true vertigo but a giddiness or light-headedness. The patient may feel unsteady, dazed, weak, or faint. However, a certain number of patients describe symptoms that are at least consonant with labyrinthine disorder; objects in the environment move momentarily, and looking upward or to the side may cause a sense of imbalance. Labyrinthine tests may show hyporeactivity of one side of the vestibular apparatus but more often they disclose no abnormalities. McHugh found a high incidence of minor abnormalities by electronystagmography, both in concussed patients and in those suffering from whiplash injuries of the neck; but we find much of the data difficult to interpret. Exceptionally, vertigo is accompanied by diminished excitability of both the labyrinth and the cochlea (deafness), and one may assume the existence of direct injury to the eighth nerve or end organ. Intolerance of alcohol is reported by some patients.


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Neurology_Adams. These physical symptoms resolve in several weeks in the majority of patients. When the symptoms persist, the patient becomes intolerant of noise, emotional excitement, and crowds. Tenseness, restlessness, fragmentation of sleep, inability to concentrate, feelings of nervousness, fatigue, worry, apprehension, and an inability to tolerate the usual amount of alcohol complete the clinical picture. The resemblance of these symptoms to those of anxiety and depression and to other forms of “posttraumatic stress disorder” is apparent.


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Neurology_Adams. The postconcussion syndrome complicates all types of head injury, mild and severe. Once established, it may persist for months or even years, and it tends to resist all varieties of treatment. Any relationship to the earlier described chronic traumatic encephalopathy is uncertain. Strangely, this syndrome is almost unknown in children under the age of approximately 6 years. Characteristic also is the augmentation of both the duration and intensity of this syndrome by problems with compensation and litigation, suggesting a psychologic factor. In countries where these matters are a less-prominent part of the social fabric, the occurrence of posttraumatic syndrome is far less frequent. Environmental stress assumes importance as well, for if too much is demanded of the patient soon after injury, irritability, insomnia, and anxiety are enhanced. In this connection, an interesting experiment was conducted by Mittenberg and colleagues (1992). A group of subjects with no personal experience


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Neurology_Adams. irritability, insomnia, and anxiety are enhanced. In this connection, an interesting experiment was conducted by Mittenberg and colleagues (1992). A group of subjects with no personal experience or knowledge of head injury was asked to select from a list of those symptoms that they would expect after a concussive head injury. They chose a cluster of features virtually identical to that of the postconcussion syndrome. The high background rates of various components of the postconcussion syndrome make it appear to be more prevalent than it truly is. The prospective study by Meares and coworkers found that, when compared to a group of patients who had noncranial trauma, the rates of the features of the syndrome were the same and that the strongest predictor of its occurrence was a previous anxiety disorder. However, the symptoms undoubtedly occur in well-adjusted, high-functioning individuals and should not be dismissed as simply anxiety.


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Neurology_Adams. An approach to treating postconcussion symptoms is given further on. It has also been reported that military personnel who experience head injuries of any degree have a higher incidence of posttraumatic stress disorder (PTSD) than those with other somatic injuries but again, the disorder is not easily predicated on psychologic factors. The same disorder can be detected in civilians after injury and it then blends clearly into the earlier-described postconcussion syndrome. Hysterical symptoms that develop after head injury, both cognitive and somatic, appear to be more common than those following injury to other parts of the body. These symptoms are discussed in Chap. 47. They may be immediate or delayed and vary from amnesia to blindness, paralysis, stuttering, inability to stand, and even to catatonia.


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Neurology_Adams. Patients with an uncomplicated concussive injury who have already regained consciousness by the time they are seen in a hospital and have a normal neurologic examination pose few difficulties in management. They should not be discharged until a decision is made about appropriate examinations (CT scans, skull films), if necessary and the results prove to be negative. Also, the patient should probably not be released until the capacity for consecutive memories has been regained and arrangements have been made for observation by the family of signs of possible, although unlikely, delayed complications (subdural and epidural hemorrhage, intracerebral bleeding, and edema). A program instituted by Mittenberg and colleagues (2001) has shown that reassurance and explanation of the concussive injury and anticipated aftereffects reduce the incidence of postconcussive symptoms at 6 months. Most such patients become mentally clear, have mild or no headache, and are found to have a normal


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Neurology_Adams. injury and anticipated aftereffects reduce the incidence of postconcussive symptoms at 6 months. Most such patients become mentally clear, have mild or no headache, and are found to have a normal neurologic examination. They do not require hospitalization or special testing, but in the current litigious climate of the United States, some form of brain imaging is nonetheless often performed as discussed in an earlier section.


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Neurology_Adams. Concussion from athletic injury currently mandates removal from play, a formal assessment of some sort and a graduated program of activity as mentioned earlier. Many testing methods and rehabilitation programs have been introduced, many of which are proprietary and not profitably recounted here.


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Neurology_Adams. Patients with persistent complaints of headache, dizziness, and nervousness, are the most difficult to manage. The main approach is to counsel patients while the symptoms resolve, coupled with a reduction in mental and physical effort that is commensurate with the patient’s level of endurance. A program must be planned in accordance with the basic problem. The notion of “cognitive rest” has been introduced but its effectiveness is difficult to gauge. Certainly youngsters and teens have difficulty concentrating on homework and other tasks and there seems to be little virtue in pressing them to perform. The range of time to recover and severity as symptoms such as “mental fog” and sleepiness is wide. If work or school work precipitate headaches, for example, plans should be made to have them curtailed. Half-time work may be suitable for some individuals but not for others. Similarly, some physical activity is to be encouraged but exertion that causes headaches or mental confusion to


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Neurology_Adams. them curtailed. Half-time work may be suitable for some individuals but not for others. Similarly, some physical activity is to be encouraged but exertion that causes headaches or mental confusion to occur or worsen should be reduced. At the same time, a bedbound or homebound state is discouraged and the patient may walk, use the Internet, watch television, or read up to the level of causing fatigue. Each of these activities is then increased at a gradual rate. In all instances, reassurance that these symptoms improve over weeks or more should be offered in order not to allow the individual to internalize the notions of chronic dementia after head injury that pervade the popular press. Some hard-driving patients return to work, only to find headache, confusion, and fatigue recur in a disabling way and must start the cycle of reduced effort over again.


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Neurology_Adams. If there is mainly an anxious depression, antidepressant medications are sometimes prescribed but this is not our usual practice—their effects are often disappointing. Simple analgesics, such as acetaminophen or nonsteroidal antiinflammatory drugs, should be prescribed for the headache. Any increase in headache, vomiting, or difficulty arousing the patient should prompt a return to the emergency department. A written instruction sheet with symptoms to be expected and clear advice about returning for examination is very helpful.


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Neurology_Adams. Litigation should be settled as soon as possible. To delay settlement usually works to the disadvantage of the patient. Long periods of observation, repetition of a multitude of tests, and waiting only reinforce the patient’s worries and fears and reduce the motivation to return to work. Neuropsychologic tests may be useful in the group with persistent cognitive difficulty, but the results should be interpreted with caution, as depression and poor motivation will degrade performance.


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Neurology_Adams. If the physician arrives at the scene of an accident and finds an unconscious patient, a rapid examination should be made before the patient is moved. First it must be determined whether the patient is breathing and has a clear airway and obtainable pulse and blood pressure, and whether there is hemorrhage from a scalp laceration or injured viscera. Severe head injuries that arrest respiration are soon followed by cessation of cardiac function. Injuries of this magnitude are often fatal; if resuscitative measures do not restore and sustain cardiopulmonary function within 4 to 5 min, the brain is usually irreparably damaged. Bleeding from the scalp can usually be controlled by a pressure bandage unless an artery is divided; then a suture becomes necessary. Resuscitative measures (artificial respiration and cardiac compression) should be continued until they are taken over by ambulance personnel. Oxygen should then be administered.


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Neurology_Adams. The likelihood of a cervical fracture–dislocation, which may be associated with any severe head injury, is the reason for taking precautions in immobilizing the neck and in moving the patient. In the awake patient, neck pain calls attention to this complication. It should be recalled that even in the absence of a spinal fracture, the spinal cord may be threatened by the instability resulting from ligamentous injuries (posing the risk of subluxation). In the study of 292 patients with traumatic cervical injuries by Demetriades and colleagues, 31 (11 percent) showed subluxations without fracture and 11 (4 percent) had cord injuries with neither fracture nor subluxation. The combined use of standard cervical spine films and cervical CT scanning detected all cervical injuries. After severe head or neck injury, even without direct impact to the neck, it is advisable under supervision to obtain standard anteroposterior, lateral, and oblique neck films, with additional gentle flexion (20


Neurology_Adams

Neurology_Adams. head or neck injury, even without direct impact to the neck, it is advisable under supervision to obtain standard anteroposterior, lateral, and oblique neck films, with additional gentle flexion (20 degrees) and extension (30 degrees) views of the neck and a neck CT scan. If these are normal and there is little or no neck pain, the cervical collar is no longer required. If after these studies, or if they cannot be obtained, or if there is significant persistent pain or other neurologic findings induced by head movement, a cervical MRI is advisable. If there are signs of a myelopathy such as flaccid legs or incontinence, urgent MRI is advisable.


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Neurology_Adams. In the hospital, the first step is to clear the airway and ensure adequate ventilation by endotracheal intubation if necessary. A search for other injuries must be made, particularly of the abdomen, chest, spine, and long bones.


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Neurology_Adams. Chesnut et al (2012), in analyzing the data from the Traumatic Coma Data Bank, found that sustained early hypotension (systolic blood pressure <90 mm Hg) was associated with a doubling of mortality. If shock was present on admission to the emergency ward, the mortality was 65 percent. Although the hypotension that follows most injuries is a vasodepressor response and usually comes under control within approximately 1 h without pressor drugs, a large, unimpeded intravenous line should be inserted. Persistent hypotension because of head injury alone is an uncommon occurrence and should always raise the suspicion of thoracic or abdominal internal bleeding, extensive fractures, or trauma to the cervical cord, or diabetes insipidus. Initially, the infused fluid should be normal saline, avoiding the administration of excessive “free water” because of its adverse effect on brain edema. Oxygen should continue to be administered until it can be shown that the arterial oxygen saturation is


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Neurology_Adams. the administration of excessive “free water” because of its adverse effect on brain edema. Oxygen should continue to be administered until it can be shown that the arterial oxygen saturation is normal.


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Neurology_Adams. A rapid neurologic survey can then be made, with attention to the depth of coma, size of the pupils and their reaction to light, ocular movements, corneal reflexes, facial movements during grimace, swallowing, vocalization, gag reflexes, muscle tone and movements of the limbs, predominant postures, reactions to pinch, and reflexes.


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Neurology_Adams. Bogginess of the temporal or postauricular area (Battle sign), bleeding from the nose or ear, and extensive conjunctival edema and hemorrhage are useful signs of an underlying basal skull fracture. However, it should be remembered that rupture of an eardrum or a blow to the nose may also cause bleeding from these parts. Fracture of the orbital bones may displace the eye, with resulting strabismus; fracture of the jaw results in malocclusion and discomfort on attempting to open the mouth. If urine is retained and the bladder is distended, a catheter should be inserted and kept there. Temperature, pulse, respiration, blood pressure, arterial oxygen saturation, and state of consciousness should be checked and charted every hour. The Glasgow Coma Scale, mentioned earlier, has provided a practical means by which the state of impaired consciousness can be evaluated at frequent intervals (see Table 34-1), but it should not be considered a substitute for a more complete neurologic


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Neurology_Adams. a practical means by which the state of impaired consciousness can be evaluated at frequent intervals (see Table 34-1), but it should not be considered a substitute for a more complete neurologic examination.


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Neurology_Adams. CT and MRI scanning of the cranium have assumed central importance at this juncture. A sizable epidural, subdural, or intracerebral blood clot is an indication for immediate surgery. The presence of contusions, brain edema, and displacement of central structures calls for measures to monitor progression of these lesions and to control ICP. These measures are best carried out in a critical care unit. Management of Raised Intracranial Pressure


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Neurology_Adams. Management of Raised Intracranial Pressure There has been a presumption, not unreasonable, that high levels of ICP are deleterious after head injury, much as it is in other processes that involve an intracranial mass. At issue has been the precise pressure at which damage occurs, whether lowering ICP improves outcome, which treatments are best, and the role of monitoring in guiding treatment. Certainly there are many biologic processes in neurons and astrocytes that greatly influence outcome after traumatic brain injury, many set in motion at the time of impact and not referable to raised ICP. At times, these overwhelm the changes induced by ICP but they are not particularly remediable, producing an emphasis on reducing ICP as a means of preventing secondary brain damage. An approach to ICP treatment is given here and also addressed in Chap. 16 on coma and Chap. 30 on brain tumors.


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Neurology_Adams. ICP monitoring In cases of moderate and severe head injury it has been the practice on most ICU services to insert one of several available devices that continuously record ICP. The rationale is ostensibly to gain control over a remediable cause of secondary brain damage, particularly if the patient’s neurologic examination is reduced to a few sentinel signs such as pupillary enlargement or because sedating medications have obscured the examination. The ventricular catheter has been considered a “gold standard” of pressure measurements as it is directly coupled to the CSF compartment, which should best reflect the summated pressures within the cranium. It has the additional advantage of affording therapeutic drainage of CSF in order to reduce ICP. In comatose patients, monitoring of ICP could avoid excessive fluid administration, refine the amount of osmotic agent and hypertonic saline used to reduce pressure, and establishes the ideal level of hyperventilation. In these respects,


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Neurology_Adams. could avoid excessive fluid administration, refine the amount of osmotic agent and hypertonic saline used to reduce pressure, and establishes the ideal level of hyperventilation. In these respects, monitoring can be helpful by guiding treatment and avoiding detrimental effects on ICP of treatments for head trauma.


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Neurology_Adams. However, there are few critical data to support the routine use of ICP monitoring. Certainly in the patient who is only drowsy or shows only minimal mass effect on CT, it is usually not necessary. Guidelines given by the American Association of Neurological Surgeons and allied groups have been that monitoring is appropriate if Glasgow Coma Scale is between 3 and 8 and there are abnormalities on CT scan, or if there is no abnormality on the CT but the patient has any two of age over 40, posturing, or has systolic blood pressure below 90 mm Hg. They set a desirable level of ICP of below 20 mm Hg and this has reinforced the role of ICP monitoring in head trauma management.


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Neurology_Adams. A reassessment of the effectiveness of ICP monitoring in a randomized trial reached the contrary conclusion that the information gained offers no advantage over clinical observation and imaging with CT scan. This trial was carried out by Chesnut and colleagues (called BEST:TRIP) in developing countries and defined raised ICP at a level that has been criticized as too low (20 mm Hg). Nevertheless, the study demonstrated that the use of a clinical approach to management of raised ICP is as feasible as a program based on direct ICP measurement. This does not negate the desirability of keeping ICP controlled at some arbitrary level; it merely questions the need for direct monitoring as a guide to management. Two trials of decompressive craniectomy (called DECRA and RESCUEicp) detailed below, used persistently raised ICP as an index for surgical treatment and in that context, ICP monitoring, of course, becomes a necessary.


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Neurology_Adams. As a practical matter, we use ICP monitoring in our unit to warn of impending deterioration from brain edema or hemorrhage if the patient cannot be effectively examined or shows poor responsiveness with evidence of mass effect on a CT scan. Although the risk of infection with a ventricular catheter is low, less than 3 percent, prolonged use may be complicated by bacterial meningitis. The catheter may be left in place for 3 to 5 days, or fewer if the clinical state and ICP are stable for 24 to 48 h. The current generation of ICP monitors employs fiberoptic strain gauges that can be inserted directly into the cerebral cortex without apparent damage.


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Neurology_Adams. General measures The first step in lowering elevated ICP is to control the incidental factors that are known to raise pressure, such as hypoxia, hypercarbia, particularly hyperthermia, awkward head positions that compress the jugular veins, and high mean airway pressures from positive pressure ventilation (see the monograph by Ropper and colleagues [2004] and Chap. 29 for further details). The avoidance of hyponatremia and serum hypoosmolarity that would allow water to enter the brain and increase its volume is accomplished by infusing only isoosmolar or hyperosmolar solutions such as normal saline. Elevations in serum osmolality as a consequence of excessive concentrations of diffusible solutes such as glucose are not useful in reducing intracranial volume because they do not create gradient for water and solutes across the cerebral vasculature. Consequently, fluids such as 5 percent dextrose in water, 0.5 normal saline, and 5 percent dextrose in 0.5 normal saline are avoided;


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Neurology_Adams. gradient for water and solutes across the cerebral vasculature. Consequently, fluids such as 5 percent dextrose in water, 0.5 normal saline, and 5 percent dextrose in 0.5 normal saline are avoided; lactated Ringer solution is permissible; normal saline, with or without added dextrose, is ideal. In a post hoc study of a cohort of severely injured patients, resuscitation with albumin was found to have a detrimental effect compared to saline (SAFE Investigators).


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Neurology_Adams. Hyperosmolar therapy The basis for this class of treatments is the creation of a gradient of water concentration from the brain to the blood that reduces brain volume. Mannitol, glycerol, and urea are effective in lowering ICP by producing serum hyperosmolarity initially and then causing a diuresis that sustains this state and secondarily causes hypernatremia and hypovolemia. Hyperosmolar saline, in contrast, raises serum sodium directly and expands intravascular volume.


Neurology_Adams

Neurology_Adams. The effects of mannitol have been of great interest to those who treat head trauma, but the ideal plan for its use has never been established. If ICP exceeds a predetermined level, for example, 20 mm Hg as recommended by aforementioned guidelines for the treatment of traumatic brain injury, mannitol 20 percent, 0.25 to 1.0 g/kg is given every 3 to 6 h to maintain serum sodium above approximately 142 mEq/L and osmolarity of 290 to 315 mOsm/L. Even if ICP monitoring is not used, an attempt may be made to maintain this level of serum osmolality for the first days after injury if contusion and brain swelling are detected on the CT scan. Mannitol in large amounts may cause renal failure, almost always reversible, though an uncertain mechanism perhaps having to do with renal blood flow. Limited evidence suggests that this complication occurs only with the use of more than 200 g of mannitol daily.


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Neurology_Adams. The relative merits of hypertonic saline and mannitol are frequently discussed and have been reviewed by one of us (Ropper, 2012). Several small series comparing the agents, referenced in the review, have shown too little difference to allow a choice between the two agents. Local experience and an overall assessment of the side effects of each typically dominate practice. Hypertonic saline (concentrations of 3 to 23 percent) has a comparable effect to mannitol in the treatment of raised ICP and has the advantage of avoiding severe dehydration because it increases osmolarity directly rather than through diuresis. The opposite also pertains, namely that patients with poor cardiac output may be subject to congestive heart failure with hypertonic saline in high volumes. Diuretics have been used to mitigate this effect. Either agent can produce a hyperglycemic, hyperosmolar state in diabetics, particularly in the elderly and in those receiving corticosteroids.


Neurology_Adams

Neurology_Adams. Hypertonic saline, 3 percent, can be used in boluses of 150 mL; a 7.5 percent solution, in 75 mL boluses; and 23 percent, in volumes of approximately 30 mL. All but the lowest concentration of saline require a central venous catheter to prevent sclerosis of veins. The same levels of sodium concentration as noted for mannitol are used as a reference to guide graduated increments of sodium administration, with serum sodium higher than about 156 mEq/L infrequently providing additional reductions in ICP.


Neurology_Adams

Neurology_Adams. Hypocarbia by hypervantilation Hypocarbia, induced by mechanical hyperventilation produces alkalosis of the CSF and cerebral vasoconstriction with a corresponding reduction in cerebral blood volume and ICP. It is effective for a limited period of time, as the pH of the spinal fluid equilibrates over hours by the elaboration of ammonium ions in the choroids plexus, allowing cerebral blood volume to return to its previous level. A single-step reduction in Pco2 typically lowers ICP for approximately 20 to 40 min. Attempts to prolong the effect of hypocarbia and the alkalosis by the intravenous administration of ammonium buffers have met with mixed success.


Neurology_Adams

Neurology_Adams. It has been suggested that hyperventilation may be harmful to some head-injured patients because of a reduction in cerebral blood flow, but the risk, if any, appears to be minimal, at least in adults. In children, reductions in cerebral blood flow have been demonstrated by Skippen and colleagues at even modest levels of hypocarbia and three-quarters show slight brain ischemia when Pco2 is below 25 mm Hg. For these reasons, hypocarbia is used in cases of head trauma mainly in acute circumstances and has been eschewed for chronic use. If the ICP continues to rise and brain swelling progresses despite these measures, the outlook for survival is poor. It should be mentioned that many patients, particularly children, hyperventilate spontaneously after head trauma.


Neurology_Adams

Neurology_Adams. Hypothermia Hypothermia and barbiturate anesthesia fairly consistently reduce ICP but relatively few patients respond to such measures for long and their clinical outcome is not improved. The main problem, aside from the difficulty maintaining lower body temperatures, is that rewarming induces substantial brain swelling and a return of ICP to prior levels or higher. An early randomized controlled trial of cooling adult patients with severe closed head injury (Glasgow Coma Scale scores of 3 to 7) to 33°C (91.4°F) for 24 h appeared to hasten neurologic recovery and may have modestly improved outcome (Marion et al), but a larger and better-conducted study led by Clifton showed that attaining hypothermia of 33°C (91.4°F) within 8 h of injury failed to improve outcome and this approach cannot be endorsed except in special circumstances. A trial reported by Andrews and colleagues came to the same conclusion when hypothermia of 32 to 35°C was added to standard treatment for raised ICP. The


Neurology_Adams

Neurology_Adams. be endorsed except in special circumstances. A trial reported by Andrews and colleagues came to the same conclusion when hypothermia of 32 to 35°C was added to standard treatment for raised ICP. The same lack of effect has been shown in studies with children (Hutchinson et al, 2008).


Neurology_Adams

Neurology_Adams. Although barbiturates lower ICP, they lower the blood pressure as well; hence, they may diminish cerebral perfusion. However, an uncontrolled series by Marshall and coworkers (1979) claimed improved survival by using barbiturates even in cases where the ICP exceeded 40 mm Hg. The more definitive randomized study by Eisenberg and associates showed no benefit from barbiturate-induced anesthesia in head-injured patients, and this class of drugs has been largely abandoned except for brief, acute control of ICP while other measures are being instituted.


Neurology_Adams

Neurology_Adams. Glucocorticoids Several controlled studies have established that the administration of high-dose steroids does not improve the clinical outcome of severe head injury. Eclipsing smaller prior studies was the well-designed Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage (CRASH) trial, conducted in more than 10,000 adults and controlled for varying degrees of injury as judged by the Glasgow Coma Scale and imaging features. The effect of the infusion of methylprednisolone 2 g, followed by 0.4 g/h for 48 h, favored survival in the untreated patients by a small but clear margin, leading to the current recommendation that steroids not be used routinely following head injury.


Neurology_Adams

Neurology_Adams. Blood pressure management The management of posttraumatic systemic hypertension represents a difficult problem. Within hours after head injury, the sympathoadrenal response and elevation of blood pressure recedes spontaneously in a matter of a few hours or days. Unless the blood pressure elevation is extreme (greater than 180/95 mm Hg), it can be disregarded in the early stages. In animal experiments, it has been found that severe hypertension leads to increased perfusion of the brain and an augmentation of the edema surrounding contusions and hemorrhages. As mentioned earlier, edema is the main element in the genesis of brain swelling and of raised ICP in most head-injured patients (Marmarou et al). This reflects a failure of autoregulatory vascular mechanisms, with resulting transudative edema in damaged areas of the brain. The control of high blood pressure must be balanced against the risk of reducing cerebral perfusion pressure and the observation that even a brief period of mild


Neurology_Adams

Neurology_Adams. edema in damaged areas of the brain. The control of high blood pressure must be balanced against the risk of reducing cerebral perfusion pressure and the observation that even a brief period of mild hypotension may provoke a cycle of cerebral vasodilatation, increased cerebral blood volume, and elevated ICP in the form of plateau waves (Rosner and Becker). Observations such as these emphasize the need for immediate correction of hypotension in severely head-injured patients.


Neurology_Adams

Neurology_Adams. Because most therapies for elevated ICP dehydrate the patient or reduce cardiac filling pressures, thereby leading to hypotension, a middle course of avoiding both severe hypertension and any degree of hypotension seems the best compromise. In lowering high levels of blood pressure, diuretics, beta-adrenergic blocking agents, or angiotensin-converting enzyme inhibitors are generally used, rather than agents that potentially dilate the cerebral vasculature (nitroglycerin and nitroprusside, hydralazine, and some of the calcium channel blockers may present this risk). Hypotension should be corrected by vasopressor agents such as phenylephrine or norepinephrine. The precise level of blood pressure that requires treatment must be judged in the context of the ICP and the presence of plateau waves, the goal being to maintain normal cerebral perfusion pressure of 60 to 80 mm Hg, as well as the patient’s previous blood pressure level; evidence of organ failure from either hyperor hypotension,


Neurology_Adams

Neurology_Adams. the goal being to maintain normal cerebral perfusion pressure of 60 to 80 mm Hg, as well as the patient’s previous blood pressure level; evidence of organ failure from either hyperor hypotension, such as cardiac or renal ischemia, must also be considered.


Neurology_Adams

Neurology_Adams. If coma persists for more than 48 h, a nasogastric tube should be passed and fluids and nutrition should be given by this route. A basilar skull fracture, especially if there is a CSF leak, may preclude this route and compel a directly situated gastric tube. Agents that reduce gastric acid production—or the equivalent, antacids by stomach tube to keep gastric acidity at a pH above 3.5—are of value in preventing gastric hemorrhage. The prophylactic use of antiepileptic drugs, as discussed earlier, under “Posttraumatic Epilepsy,” recently has been favored, but there is no evidence that delayed epileptic seizures are reduced (see Chang and Lowenstein). Only if there has been a seizure are antiepileptics given.


Neurology_Adams

Neurology_Adams. Restlessness is controlled by diazepam, propofol, or a similar drug, but only if careful nursing fails to quiet the patient and provide sleep for a few hours at a time. Etomidate and dexmedetomidine may be preferable for reducing agitation because they are minimally sedating. Fever is counteracted by antipyretics such as acetaminophen and, if necessary, by a cooling blanket. The use of morphine or bromocriptine to quiet episodes of vigorous extensor posturing and accompanying adrenergic activity already has been mentioned.


Neurology_Adams

Neurology_Adams. The need for surgical intervention during the acute posttraumatic period is decided by two factors: the clinical status of the patient and the findings on imaging. The presence of a subdural or epidural clot that is causing a shift of central brain structures calls for evacuation of the collection. The approach to these lesions has been discussed earlier. Should the elevated ICP not respond to this procedure or to the standard osmotic agents and other medical measures outlined earlier, or should the condition of the patient and vital signs then begin to deteriorate (heart rate rising, temperature rising or falling below normal, state of consciousness worsening, hemiplegia, plantar reflexes more clearly extensor), a renewed search must be undertaken for a late-occurring cerebral hemorrhage. Usually in these clinical circumstances, CT scanning will disclose a new or enlarged epidural, subdural, or intracerebral hematoma, or worsened cerebral edema. If death or severe disability is to be


Neurology_Adams

Neurology_Adams. Usually in these clinical circumstances, CT scanning will disclose a new or enlarged epidural, subdural, or intracerebral hematoma, or worsened cerebral edema. If death or severe disability is to be avoided, operation in these cases must be undertaken before the advanced signs of brainstem compression—decerebrate or decorticate posturing, hypertension, bradycardia—have appeared.


Neurology_Adams

Neurology_Adams. The use of decompressive craniectomy in patients with progressive and intractable traumatic brain swelling has been a subject of renewed interest, after having been practically abandoned several decades ago. Guerra and colleagues reported on 57 such patients, mostly young adults, who underwent wide frontotemporal craniectomy, unilateral in 31 and bilateral in 26. Of these, 58 percent attained surprisingly good states of rehabilitation. These authors were of the opinion that these results represented a significant improvement over the expected outcome in this particular group of patients. A similar open trial conducted by Aarabi and colleagues described 40 percent with good outcome. Similar results in children were reported by Polin and associates. The few cases with which we have been involved, mostly children operated late, have not been as encouraging.


Neurology_Adams

Neurology_Adams. However, these generally favorable results could not be validated in the randomized DECRA trial carried out by Cooper and colleagues, or in the trial reported by Cooper and coworkers. Decompression did indeed reduce ICP, as expected, when the intracranial contents are exposed to atmospheric pressure, but surgery did not improve outcome and in the latter trial, outcome was worse with decompression. Rounding out these trials is the one reported by Hutchinson and colleagues (2016) of patients with refractory intracranial hypertension that showed higher rates of survival but also higher rates of vegetative state with decompression. The details of the operations and choice of ICP level that were chosen to trigger operation have been criticized in each of these trials, but they remain the best information to date and broadly but paradoxically do not favor indiscriminate decompression to reduce ICP. A review of intracranial hypertension that appeared soon after the DECRA trial is provided by


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Neurology_Adams. Stochetti and Maas. The treatment of the general medical diseases relating to protracted coma was outlined in Chap. 16. Each patient presents unique problems.


Neurology_Adams

Neurology_Adams. As has been intimated, the outcome in severe injury is particularly discouraging, more so with increasing age. Some aspects of prognosis were mentioned earlier but the following general comments serve to frame the problem. In the survey of the large European Brain Injury Consortium, comprising 10,005 adult patients, the injury proved fatal in 31 percent; 3 percent were left in a persistent vegetative state, and 16 percent remained severely disabled neurologically (Murray et al). Data from the extensively analyzed Traumatic Coma Data Bank are comparable, as reported by Marshall and coworkers (1983). The signs of focal brain disease, whether because of closed head injuries or open and penetrating ones, tend always to ameliorate as the months pass. A hemiplegia is often reduced to a minimal hemiparesis or to ineptitude of voluntary motor function with exaggerated reflexes and an equivocal Babinski sign on that side, and aphasia is gradually transformed into a stuttering or hesitant


Neurology_Adams

Neurology_Adams. hemiparesis or to ineptitude of voluntary motor function with exaggerated reflexes and an equivocal Babinski sign on that side, and aphasia is gradually transformed into a stuttering or hesitant paraphasia or dysnomia that is not disabling. Many of the signs of brainstem disease (cranial nerve dysfunction and ataxia) improve also, usually within the first 6 months after injury (Jennett and Bond) and often to a surprising extent. Most patients who had been in coma for many hours or days—that is, those with severe brain injuries—are left with memory impairment and other cognitive defects and with personality changes. These may be the only lasting sequelae as detailed earlier. According to Jennett and Bond, these mental and personality changes are a greater handicap than focal neurologic ones as far as social adjustment is concerned. In open head wounds and penetrating brain injuries, Grafman and coworkers found that the magnitude of tissue loss and location of the lesion were the main


Neurology_Adams

Neurology_Adams. as far as social adjustment is concerned. In open head wounds and penetrating brain injuries, Grafman and coworkers found that the magnitude of tissue loss and location of the lesion were the main factors affecting the outcome.


Neurology_Adams

Neurology_Adams. The prognosis of head injury is influenced by several other factors as mentioned. The age of the patient is the most important factor (Vollmer et al). Increasing age reduces the chances of survival and of good recovery. Older patients often remain disabled, especially when compensation is involved. Young and middle-aged patients do better, particularly if they are not entitled to compensation.


Neurology_Adams

Neurology_Adams. As a general statement, children recover more completely than adults. Russell pointed out long ago that the severity of the injury as measured by the duration of traumatic amnesia is a useful prognostic index. Of patients with a period of amnesia lasting less than 1 h, 95 percent were back at work within 2 months; if the amnesia lasted longer than 24 h, only 80 percent had returned to work within 6 months. However, approximately 60 percent of the patients in his large series still had symptoms at the end of 2 months, and 40 percent at the end of 18 months. Of the most severely injured (those comatose for several days), many remained permanently disabled. However, the degree of recovery was often better than one had expected; the motor impairment, aphasia, and dementia tended to lessen and sometimes cleared. Improvement could continue over a period of 3 or more years. Obviously, multiple-organ injury and, particularly, hypotension in the hours immediately after injury, have major


Neurology_Adams

Neurology_Adams. and sometimes cleared. Improvement could continue over a period of 3 or more years. Obviously, multiple-organ injury and, particularly, hypotension in the hours immediately after injury, have major effects, not just on survival, but in some studies, with neurocognitive and behavioral outcome.


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Neurology_Adams. The remarkable findings of voluntary activation of parts of the cerebral cortex in patients who are in a vegetative or minimally conscious state were mentioned earlier and in Chap. 16. These serve as a caution to the neurologist to assign the diagnostic labels of vegetative and minimally conscious state only after careful and preferably, repeated examinations and then to temper communication with the family and other physicians by an appropriate degree of uncertainty as to outcome. Nonetheless, most patients who are vegetative for 6 or more months after cranial trauma will not recover to a meaningfully independent life. Aarabi B, Hesdorffer DC, Ahn ES, et al: Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg 104:469, 2006. Adams JH, Graham DI, Jennet B: The neuropathology of the vegetative state after an acute brain insult. Brain 123:1327, 2000.


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Neurology_Adams. Adams JH, Graham DI, Jennet B: The neuropathology of the vegetative state after an acute brain insult. Brain 123:1327, 2000. Adams JH, Graham DI, Murray LS, Scott G: Diffuse axonal injury due to nonmissile head injury in humans: An analysis of 45 cases. Ann Neurol 12:557, 1982. Albu S, Florian IS, Bolboaca SD: The benefit of early lumbar drain insertion in reducing the length of CSF leak in traumatic rhinorrhea. Clin Neurol Neurosurg 142:43, 2016. Andrews PJ, Sinclair HL, Rodriguez A, et al: Hypothermia for intracranial hypertension after traumatic brain injury. N Engl J Med 373:2403, 2015. Annegers JF, Grabow JD, Groover RV, et al: Seizures after head trauma: A population study. Neurology 30:683, 1980. Annegers JF, Hauser A, Coan SP, Rocca WA: A population-based study of seizures after traumatic brain injuries. N Engl J Med 338:20, 1998. Ascroft RB: Traumatic epilepsy after gunshot wounds of the head. Br Med J 1:739, 1941.


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Neurology_Adams. Ascroft RB: Traumatic epilepsy after gunshot wounds of the head. Br Med J 1:739, 1941. Baugley IJ, Nicholls JL, Felmingham KL, et al: Dysautonomia after traumatic brain injury: A forgotten syndrome. J Neurol Neurosurg Psychiatry 67:39, 1999. Bender MB, Christoff N: Nonsurgical treatment of subdural hematomas. Arch Neurol 31:73, 1974. Bonnier C, Nassogne MC, Saint-Martin C, et al: Neuroimaging of intraparenchymal lesions predicts outcome in shaken baby syndrome. Pediatrics 112:808, 2003. Boto GR, Lobato RD, Rivas JJ, et al: Basal ganglia hematomas in severely head injured patients: Clinicoradiological analysis of 37 cases. J Neurosurg 94:224, 2001. Bowman KM, Blau A, Reich R: Psychiatric states following head injury in adults and children. In: Feiring EH (ed): Brock’s Injuries of the Brain and Spinal Cord and Their Coverings, 5th ed. New York, Springer-Verlag, 1974, pp 570–613.


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Neurology_Adams. Cairns H: Injuries of frontal and ethmoid sinuses with special reference to CSF rhinorrhea and aerocele. J Laryngol Otol 52: 289, 1937. Casson IR, Sham RAJ, Campbell EA, et al: Neurological and CT evaluation of knocked-out boxers. J Neurol Neurosurg Psychiatry 45:170, 1982. Caveness WF: Onset and cessation of fits following craniocerebral trauma. J Neurosurg 20:570, 1963. Caveness WF: Post-traumatic sequelae. In: Caveness WF, Walker AE (eds): Head Injury. Philadelphia, Lippincott, 1966, pp 209–219. Caviness VS Jr: Epilepsy and craniocerebral injury of warfare. In: Caveness WF, Walker AE (eds): Head Injury. Philadelphia, Lippincott, 1966, pp 220–234. Chang BS, Lowenstein DH: Practice parameter: Antiepileptic drug prophylaxis in severe traumatic brain injury. Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 60:10, 2003.