Coma, Head Trauma, and Spinal Cord Injury



Coma, Head Trauma, and Spinal Cord Injury


Galen V. Henderson



COMA


Background


Impaired States of Consciousness



  • 1. Coma describes total or near-total unresponsiveness. It is a sleep-like state of unconsciousness from which the patient cannot be aroused by external or internal stimuli. The degree of coma varies; in its deepest stage, no reaction of any kind is obtainable; corneal, papillary, and pharyngeal responses are absent. With lesser degrees, there is slight stirring to stimuli and brainstem reflexes are preserved. In such lighter stages of coma, sometimes referred to by the ambiguous and unhelpful terms semicoma or obtundation, most of the brainstem reflexes can be elicited. Respiration rate and pattern also vary with the depth of coma.


  • 2. Stupor refers to a state in which the patient can be only transiently roused by vigorous and repeated stimuli, but arousal cannot be sustained without repeated stimulation. Verbal output is unintelligible or absent, and there is some purposeful movement to noxious stimulation. Restless or stereotyped motor activity is common and there is a reduction of the natural shifting of body positions.


  • 3. Drowsiness and lethargy denote reduced wakefulness resembling sleep that allows easy and usually sustained arousal.


  • 4. Confusion refers to impaired attention and implies inadequate arousal to sustain coherent thoughts and actions.


  • 5. Delirium, as used by neurologists, usually refers to a state of confusion with periods of agitation and sometimes hypervigilance, active irritability, and hallucinations, typically alternating with periods during which the level of arousal is depressed.


Pathophysiology



  • 1. Excitatory inputs emanating from the midbrain and rostral pons (resticular-activating system [RAS]) ascend to the thalamus, exciting thalamocortical neurons of the thalamic intralaminar, and midline nuclei. The neurons project widely throughout the cerebral cortex and this RAS supports arousal. The anatomic boundaries of the upper brainstem RAS are indistinct.


  • 2. These ascending reticulothalamic neurons have cholinergic activity.


  • 3. The act of attention is conceived as depending on both the diffuse arousal system and cortical systems for directed attention in various spheres:



    • a. Posterior parietal lobes (sensory awareness).


    • b. Frontal association cortex (motor attention: directed movements of the eyes, limbs, and body).


    • c. Cingulate cortex (motivational aspects of attention).


    • d. Lesions that affect these areas cause global inattention and confusional states.


    • e. Acute confusional states are therefore due to



      • 1) Diffuse disease in the cerebral cortex


      • 2) Focal lesions in various regions of the cortex



      • 3) Thalamic cortical connections


      • 4) Forebrain and subcortical structures.


Diagnosis


Clinical Presentation



  • 1. The primary goal of the examination of the unresponsive patient is to determine the cause of destruction of brain tissue as, for example, from cerebral hemorrhage or from metabolic disturbances that are extrinsic to the brain, such as uremic or hypoglycemic encephalopathy.


  • 2. The electroencephalogram (EEG) reflects cortical and thalamic neurophysiologic function and is helpful in determining the level of cerebral disturbance and disease progression.


  • 3. The Glasgow Coma Scale (GCS; Table 1-1) is a standardized instrument designed for rapid assessment and communication about patients who have traumatic brain injury (TBI).



    • a. This scale measures the patient’s best response in three areas: eye opening, motor activity, and language.


    • b. GCS scores range from 3 to 15. When the total score is 8 or less, the patient is usually comatose.


Components of the Examination



  • 1. Observing the patient yields considerable information. The predominant postures of the limbs and body; the presence or absence of spontaneous movements on each side; the position of the head and eyes; and the rate, depth, and rhythm of respirations give substantial formation.



    • a. Level of consciousness is measured by the patient’s reaction to:



      • 1) Calling name


      • 2) Simple commands


      • 3) Progressively intense noxious stimuli such as tickling the nares, supraorbital or sternal pressure, pinching the side of the neck or inner parts of the arms or thighs, or applying pressure to the knuckles


  • 2. Examination of the pupils is of great diagnostic importance



    • a. Normal pupillary size, shape, and light reflexes indicate integrity of the midbrain structures and therefore direct attention to a cause of coma other than destruction or secondary compression of this area by a hemispheral mass.


    • b. Pupillary reactions are diminished with rostral midbrain lesions.



      • 1) A unilaterally enlarged pupil (>5.5 mm) is an early indicator of stretching or compression of the third nerve and reflects a cerebral mass on that side.


      • 2) Loss of light reaction usually precedes enlargement of the pupil.








        TABLE 1-1 Glasgow Coma Scale






































        Points


        Eye Opening


        Verbal


        Motor


        6




        Obeys


        5



        Oriented


        Localizes to pain


        4


        Spontaneous


        Confused


        Withdraws to pain


        3


        To speech


        Inappropriate


        Flexion (decorticate)


        2


        To pain


        Unintelligible


        Extensor (decerebrate)


        1


        None


        None


        None




      • 3) The pupil may become oval or pear-shaped, and may appear to be off center (corectopia) because of differential loss of innervation of portions of the pupillary sphincter.


      • 4) As midbrain displacement continues from a mass lesion, both pupils dilate and become unreactive to light, probably from compression of the oculomotor nuclei in the rostral midbrain.


      • 5) As the upper brainstem is further compressed, there tends to be a slight reduction in pupillary size on both sides to 5 mm or smaller.


    • c. Pupillary reactions with pontine lesions.



      • 1) Pontine lesions cause miotic pupils less than 1 mm in diameter with barely perceptible reaction to strong light.



        • a) The Horner syndrome (miosis and ptosis) may be observed ipsilateral to the lesions of the brainstem or hypothalamus or as a sign of dissection of the internal carotid artery.


    • d. Coma caused by drug intoxications and intrinsic metabolic disorders spares pupillary reactions, but there are several exceptions.



      • 1) High concentrations of opiates cause coma and very small pupils that are barely light reactive.


      • 2) High-dose barbiturates may act similarly, but the pupillary diameter tends to be 1 mm or more.


      • 3) Systemic poisoning with atropine or with drugs that have atropinic qualities, for example, tricyclic antidepressants, is characterized by wide dilatation and fixity of the pupils.


      • 4) Hippus or fluctuating pupillary size is characteristic of metabolic encephalopathy.


  • 3. Movements of the eyes, eyelids and corneal response



    • a. In light coma of metabolic origin, the eyes rove conjugately from side to side in seemingly random fashion, sometimes resting briefly in an eccentric position.


    • b. These movements disappear as coma deepens, and the eyes then remain motionless and slightly exotropic.


    • c. Lateral and downward deviation of one eye suggests the presence of a third nerve palsy, and medial monocular deviation, a sixth nerve palsy.


    • d. Persistent conjugate deviation of the eyes to one side (gaze deviation) is away from the side of paralysis with a large cerebral lesion (looking toward the lesion) and toward the side of the paralysis with a unilateral pontine lesion (looking away from the lesion).


    • e. “Wrong-way” conjugate deviation may occur with thalamic and upper brainstem lesions.


    • f. During a focal seizure the eyes turn or jerk toward the convulsing side (opposite to the irritative focus).


    • g. The globes turn down and inward (looking at the nose) with hematomas or ischemic lesions of the thalamus and upper midbrain.


    • h. Retraction and convergence nystagmus occurs with lesions in the tegmentum of the midbrain.


    • i. Ocular bobbing (rapid downward and slower upward movements) accompanies bilateral horizontal gaze paresis with damage to the pons.


    • j. Ocular dipping (slow downward and return rapidly to the meridian) is observed with coma caused by anoxia and drug intoxications.


    • k. Coma producing structural lesions of the brainstem abolish most if not all conjugate ocular movements, whereas metabolic disorders generally do not (except for certain deep drug intoxications, particularly from antiepileptic medications).


    • l. Oculocephalic reflexes (doll’s eye movements) are elicited by brisk turning of the head. The response in coma of metabolic origin or that caused by bihemispheric structural lesions consists of conjugate movements of the eyes in the opposite direction.



    • m. Elicitation of these ocular reflexes in a comatose patient provides two pieces of information:



      • 1) Evidence of unimpeded function of the midbrain and pontine tegmental structures that integrate ocular movements and of the ocular motor nerves.


      • 2) Loss of the cortical inhibition that normally holds these movements in check.


    • n. Asymmetry of elicited eye movements remains a dependable sign of focal brainstem disease. In coma caused by a large mass in one cerebral hemisphere that secondarily compresses the upper brainstem, the oculocephalic reflexes are usually present, but adduction of the eye on the side of the mass is impeded as a result of a compressive third nerve paresis.


    • o. Irrigation of one ear with 10 mL of cold water causes slow conjugate deviation of the eyes toward the irrigated ear, followed in a few seconds by a compensatory nystagmus (fast component away from the stimulated side). This is the vestibuloocular, oculovestibular, or caloric test.


    • p. The ears are irrigated separately, several minutes apart. In the comatose patient, the corrective phase of the nystagmus is lost and the eyes are tonically deflected to the side of irrigation with cold water. This position may be held for 2 to 3 minutes.


    • q. Brainstem lesions disrupt these vestibuloocular reflexes (VOR); if one eye abducts and the other fails to, one can conclude that the medial longitudinal fasciculus has been interrupted.


    • r. Abducens palsy is indicated by an esotropic resting position and a lack of outward deviation of one eye with the reflex maneuvers.


    • s. Complete absence of ocular movement in response to oculovestibular testing indicates a severe disruption of brainstem tegmental system in the pons or midbrain.


  • 4. A reduction in the frequency and eventual loss of spontaneous blinking; then a loss of response to touching the eyelashes, and finally, a lack of response to corneal touch (the signs of deepening coma). A marked asymmetry in corneal responses indicates either an acute lesion of the opposite hemisphere or less often, an ipsilateral lesion in the brainstem.


  • 5. Skeletal motor and reflex signs



    • a. Restless movements of all the limbs and grasping and picking movements signify that the corticospinal tracts are more or less intact. Oppositional resistance to passive movements (paratonic rigidity), complex avoidance movements, and discrete protective movements has the same meaning. Abduction movements (away from midline) have the same significance and differentiate a motor response from posturing. Patients who have hemispheric lesions typically lie in comfortable-appearing, relatively normal postures.


    • b. Patients who have brainstem lesions often display abnormal postures. The symmetry of spontaneous movement may give a clue to the side of a focal lesion.


    • c. The terms “decorticate” and “decerebrate rigidity” refer to experimental studies of animals and do not accurately reflect the clinicopathologic correlations that they imply.



      • 1) Decorticate posturing: Lower extremity extension and internal rotation with flexion of both upper extremities.


      • 2) Decerebrate posturing: Lower and upper extremity extension.


    • d. Upper extremity flexion reflects more superficial, less severe, and more chronic lesions at the level of the diencephalon or above. Upper and lower extremity extension often accompanies brainstem lesions; however, as mentioned, the upper extremity extension depends on the degree and acuteness of the lesion and being reflexively driven, on the stimulus applied at the time of the examination. The responsible lesions may also be reversible, as in severe toxic and metabolic encephalopathies.



    • e. Exaggerated deep tendon reflexes and extensor plantar responses also suggest a lateralized lesion, but they may be misleading.


    • f. Careful observation for subtle movements suggesting seizures should be sought in all cases of coma; these implicate nonconvulsive status epilepticus as the cause of coma.


  • 6. Respiratory patterns



    • a. Hyperventilation is common and has poor localizing value. Differential diagnosis includes



      • 1) Fever


      • 2) Sepsis


      • 3) Metabolic acidosis


      • 4) Drug toxicity


      • 5) Cardiopulmonary disease


    • b. Cheyne-Stokes respirations refers to a periodic breathing pattern of alternating hyperpnea and apnea.


    • c. Apneustic breathing



      • 1) Characterized by a prolonged pause at the end of inspiration and is also called “inspiratory cramp” (a pause of 2 to 3 seconds in full inspiration). This localizes to a lesion in the mid-to-caudal pons.


    • d. Biot breathing (ataxic breathing)



      • 1) Characterized by chaotic or ataxic breathing pattern with loss of regularity of alternating pace and depth of inspirations and expirations that may occur when the neurons in the respiratory center are damaged.


      • 2) This pattern progresses to one of intermittent prolonged inspiratory gasps that are recognized by all physicians as agonal in nature, and finally to apnea. In fact, respiratory arrest is the mode of death of most patients with serious central nervous system disease. A variety of lesions cause this pattern terminally.


Reason for Decreased Level of Consciousness with Structural Lesions



  • 1. Structural coma can result from diffuse or bilateral cerebral hemispheric or primary brainstem involvement.



    • a. Purely unilateral cerebral lesions do not produce coma.


    • b. Loss of consciousness from unilateral cerebral lesions indicates pressure or displacement of the opposite hemisphere or upper brainstem.


    • c. Persisting loss of consciousness from cerebral hemispheric disease indicates bilateral cerebral hemispheric damage.


  • 2. As the mass effect progresses, it causes displacement of the upper brainstem through the tentorial notch—herniation—thereby interrupting activity ascending to the cerebral hemisphere from the RAS.



    • a. Secondary hemorrhages occur in the brainstem tegmentum, in contrast to primary brainstem hemorrhage, which is usually in the base of the pons.


    • b. Secondary ischemic and hemorrhagic lesions lead to permanent coma and brainstem tegmental signs involving eye movements and pupils.


    • c. Supratentorial tissue shifts may compress the posterior cerebral arteries against the incisura of the tentorium, causing infarction of the occipital lobes. Patients may survive this compressive effect to be left with visual-field defects or blindness from damage to the occipital lobes.


Locked-in Syndrome



  • 1. Lesion is located bilaterally in the base of the pons.


  • 2. The patient is awake, has lost horizontal eye movements, and is unable to talk or move the arms or legs. The patient is therefore “de-efferented” but remains conscious.



    • a. The only way the patient can express alertness and communication is through eyelid and vertical eye movements.



    • b. Midbrain involvement can also cause the locked-in syndrome accompanied by bilateral ptosis and third nerve palsies. The only clue that the patient is conscious is some remnant of movement such as the orbicularis oculi in response to command.


    • c. These patients require meticulous nursing and psychological care.


    • d. Survival may be prolonged, and recovery is possible in patients depending on the lesion type and extent of damage.


Vegetative State



  • 1. Coma after an acute event that damages the hemispheres diffusely seldom lasts more than 2 to 4 weeks and most patients transition to the vegetative state. These patients exhibit wakefulness but not consciousness; they open their eyes in response to painful stimuli or spontaneously and may blink to threat. Caloric and oculocephalic movements are retained. Intermittently, the eyes may move from side to side seemingly following objects or fixate momentarily on the physician or a family member giving the erroneous impression of recognition. Respirations may quicken in response to stimulation and certain automatisms such as swallowing, bruxism, grimacing, grunting, and moaning may be observed. However, the patient remains totally inattentive, does not speak, and show no signs of awareness of the environment or inner need; responsiveness is limited to primitive or inner need and primitive postural reflexes movements of the limbs. There is loss of sphincter control. There may be arousal or wakefulness in alternation cycles as reflected in partial eye opening, but the patient regains neither awareness nor purposeful behavior of any kind.


  • 2. Minimally conscious state is a recently defined category in which the patient retains minor and often intermittent function such as moving a limb to command, making facial expressions or tracking visually, sometimes to command and at other times, spontaneously. It is separated from vegetative state and from other states of severe disability.


Psychogenic Unresponsiveness

The eye movements are particularly helpful in distinguishing psychogenic unresponsiveness and catatonia from coma and the vegetative state.



  • 1. If the patient lies with the eyes closed, lifting the eyelids results in a slow closure in genuine coma but rapid or forceful closure of the eyes demonstrates responsiveness.


  • 2. Smooth roving eye movements cannot be produced voluntarily.


  • 3. Caloric testing elicits nystagmus in psychogenic coma but not in metabolic or structural coma. Occasional patients who feign unresponsiveness can inhibit caloric-induced nystagmus by concentrated visual fixation. However, they do not exhibit deviation of the eyes without nystagmus fast phases, as the comatose patient does. Similarly, in psychogenic coma during oculocephalic maneuvers, visual fixation enhances the VOR so that the eyes move in the orbit, stabilizing the gaze in one spot. In comatose patients, the VOR may be hypoactive or lost with deep metabolic coma or with structural lesions in the pontine tegmentum.


  • 4. Patients with psychogenic unresponsiveness often look away from the examiner, toward the mattress.


Treatment


Approach to Patient



  • 1. As with all acutely ill patients, the approach to the comatose patient should follow a rapid and prioritized algorithm that ensures stabilization of vital functions
    and rapid assessment and therapy for potential disorders that threaten life (Tables 1-2 and 1-3).








    TABLE 1-2 Approach to the Assessment and Management of Acute Coma

















    Stabilization




    • Airway control



    • Oxygenation and ventilation



    • Adequate circulation (includes avoidance of hypotension in strokes)



    • Cervical spine stabilization


    Immediate therapies given to all patients




    • Thiamine 100 mg IV



    • Dextrose 50% 50 mL IV (may be held if immediate finger stick glucose establishes adequate serum glucose)



    • Naloxone 0.4-2 mg IV (may be repeated)



    • Obtain blood for CBC, PT/PTT, chemistry panel, toxic screen, blood cultures, anticonvulsant levels


    Threatening conditions to be considered for possible early therapy




    • Elevated ICP → head CT



    • Meningitis, encephalitis, or both → antibiotics, LP, blood cultures



    • Myocardial infarction → ECG



    • Hypertensive encephalopathy → early therapy



    • Status epilepticus → EEG



    • Acute stroke → consider thrombolytic therapy


    IV, intravenous; CBC, complete blood count; PT, prothrombin time; PTT, partial thromboplastin time; ICP, intracranial pressure; CT, computed tomography; LP, lumbar puncture; ECG, electrocardiogram; EEG, electroencephalogram. From Neurologic Clinics, Neurologic Emergencies, May 1998, with permission.



  • 2. The ABCs (airway, breathing, and circulation) of acute resuscitation top the list.


  • 3. Acute cervical stabilization is crucial whenever there is any possibility of cervical trauma or spinal instability caused by medical disease, as in rheumatoid arthritis.


  • 4. Maneuvers that require neck movement should be modified to minimize movements or should be avoided (oculocephalics stimulation) until after adequate radiographs have eliminated any concern of cervical instability.


TRAUMATIC BRAIN INJURY


Background



  • 1. In the Western world, trauma is the leading cause of death and disability in children and adults from ages 1 to 44.


  • 2. Head injuries account for most morbidity and mortality from trauma and are responsible for over half of the trauma-related deaths.


  • 3. The incidence of TBI peaks in the 15- to 24-year-old age group; males are affected more commonly than are females.









    TABLE 1-3 Main Causes of Coma




















































































































    1. Focal disease



    a. Trauma (contusion, ICH)



    b. Nontraumatic ICH



    c. Ischemic stroke



    d. Infection (abscess, subdural empyema, focal encephalitis)



    e. Tumor



    f. Demyelination (MS, ADEM)


    2. Nonfocal disease



    a. Trauma (elevated ICP, diffuse axonal injury)



    b. Vascular syndromes




    1) SAH




    2) Aneurysm in posterior fossa with mass effect




    3) Hypoxic-ischemic encephalopathy




    4) Stroke (focal strokes with nonfocal presentations, posterior fossa infarct with mass effect, hydrocephalus)




    5) Hypertensive encephalopathy



    c. Infection (meningitis, diffuse encephalitis)



    d. Tumor related




    1) Tumor (brainstem invasion, posterior fossa mass, elevated ICP, and hydrocephalus), paraneoplastic syndromes (brainstem encephalitis, vasculitis)



    e. Toxic and metabolic




    1) Toxic




    2) Metabolic




    3) Withdrawal symptoms




    4) Nutritional deficiencies




    5) Disordered temperature regulation



    f. Seizures (postictal state, nonconvulsive status epilepticus)



    g. Others




    1) Basilar migraines




    2) Transient global amnesia




    3) TTP and other syndromes of medical illness




    4) Sleep deprivation




    5) Situational (i.e., ICU psychosis)




    6) Psychiatric (conversion, depression, mania, catatonia)


    ICH, intracranial hemorrhage; MS, multiple sclerosis; ADEM, acute disseminated encephalomyelitis; ICP, intracranial pressure; ICU, intensive care unit; SAH, subarachnoid hemorrhage; TTP, thrombotic thrombocytopenic purpura. From Neurologic Clinics, Neurologic Emergencies, May 1998, with permission.



  • 4. There are approximately 1.5 million new brain injuries annually in the United States and every year, approximately 52,000 deaths occur from TBI.


  • 5. Rates of TBI-related hospitalization have declined nearly 50% since 1980, a phenomenon that may be attributed, in part, to successes in injury prevention, high-quality prehospital paramedic systems, helicopter transport systems, and comprehensive acute care in an intensive care unit (ICU).


  • 6. Approximately 200,000 patients experience severe TBI (i.e., present in coma); 80,000 to 90,000 survive with varying degrees of disability.



    • a. In 1993 the reported mortality from the Traumatic Coma Data Bank (TCDB) was about 33%.



    • b. While some suggest that contemporary management of patients with severe TBI should limit the mortality rate to approximately 20%, leaving only 50,000 deaths per year, some continue to report mortality rates as high as 37%, 51%, or 60%.


  • 7. The direct cost estimate is around $4 billion annually.


Pathophysiology



  • 1. TBI is a heterogeneous pathologic entity.


  • 2. TBI has primary and secondary components.



    • a. Primary injuries are the result of mechanical events such as acceleration, deceleration, rotational, penetrating, and blunt forces that occur at the moment of impact. Injury to the blood vessels is evident by small tissue hemorrhages, intracerebral, subdural, or epidural hematomas (EDHs) all of which can in turn result in secondary injury. Coronal translational forces are more apt to produce widespread axonal injuries. Patients with diffuse axonal injury (DAI) are less likely to have increased intracranial pressure and lucid intervals. Amyloid precursor protein topography shows that axons in the corpus callosum and fornices are the most susceptible to injury.


    • b. Secondary injuries are due to biochemical reactions and cascades that can occur from the time of the initial event to minutes, hours, and even days after primary injury particularly from pulmonary and circulatory physiologic abnormalities. For example, the occurrence of hypotension, with or without hypoxia, doubles the mortality and increases the morbidity of severe head injury. Hypotension occurring in the initial phase of resuscitation is associated with increased mortality, even when episodes are relatively brief. About 6% of patients with severe TBI as the main presenting feature also have a cervical spine injury. About 24% of patients with cervical spine injury as the main presenting feature also have a TBI.


Scalp Laceration



  • 1. Tend to bleed profusely because of the ample blood supply and poor vasoconstrictive ability of the scalp vasculature.


  • 2. They should be inspected, palpated, irrigated, debrided, and sutured.


Skull Fractures



  • 1. Linear fractures are usually benign unless they occur in the area of (or involve) the middle meningeal artery or dural sinus, which may result in epidural or subdural hemorrhages, respectively.


  • 2. Depressed fractures may cause dural tears and injury to underlying brain tissue.


  • 3. Comminuted fractures are multiple linear fractures with depression at the site of impact.


Basal Skull Fractures



  • 1. Linear fractures extend into the anterior, middle, or posterior cranial fossa at the skull base.


  • 2. They are often difficult to visualize on plain skull films or axial computed tomography (CT) scans. The diagnosis is often based on clinical signs and symptoms.


  • 3. There is a risk of meningitis if the dura is penetrated; however, prophylactic antibiotics are not indicated.


  • 4. Anterior fossa fractures generally involve the frontal bone and ethmoid and frontal sinuses.



    • a. Characterized by bilateral periorbital ecchymosis (“raccoon eyes”).


    • b. Anosmia from damage to the olfactory apparatus is common.



    • c. Rhinorrhea occurs in 25% of patients, usually lasts 2 to 3 days, and is often self-limiting with conservative measures (e.g., elevating the head of the bed, cautioning the patient against blowing nose, and lumbar drain placement).


  • 5. Middle fossa fractures are characterized by ecchymosis over the mastoid process behind the ear that may not appear for up to 24 hours (Battle sign) and otorrhea.



    • a. Otorrhea indicates tympanic membrane rupture that allows free flow of cerebrospinal fluid (CSF) through the ear; this problem is often self-limiting with conservative measures (e.g., elevating the head of the bed).


    • b. May be associated with cranial nerve VI, VII, and VIII palsies.


  • 6. Avoid inserting a nasogastric tube into a patient with a suspected basal skull fracture.



    • a. This warning should probably be applied to all comatose patients with TBI until the presence of basal fracture has been addressed.


    • b. Use an orogastric tube instead.


Concussion



  • 1. Patients may or may not have loss of consciousness; being “stunned,” confused, having their “bell rung” are equivalents of concussion.


  • 2. Retrograde and anterograde amnesias are common.


  • 3. There are guidelines for the performance of CT scanning after concussion. Vomiting, older age, presence of fracture on examination, and dangerous mechanism of injury are all predictive of finding a cerebral lesion if CT is done.


  • 4. Patients commonly complain of subsequent headache, dizziness, irritability, short-term memory loss, fatigue, and reduced attention span. These “minor” head injuries may have sequelae that may greatly disrupt activities of daily living (postconcussive syndrome).


Cerebral Contusion



  • 1. Contusion is bruising of brain tissue and does not occupy much space in the beginning but may blossom within 24 to 48 hours after injury days and cause significant intracranial hypertension. They most commonly involve the tips of the frontal and temporal lobes.


  • 2. Contusions may be caused by coup or contrecoup injuries.


  • 3. It is important to check coagulation studies (e.g., prothrombin and partial thromboplastin times) and platelet counts and to correct clinically important abnormalities with fresh frozen plasma and platelet than fusions.


Subdural Hematoma



  • 1. Classification



    • a. “Acute” is used for those less than 3 days old.


    • b. “Subacute” for age 3 days to 3 weeks old.


    • c. “Chronic” more than 3 weeks from injury.


  • 2. Acute subdural hematoma (ASDH) is the most common traumatic intracranial hematoma (35% to 40% of patients with severe TBI) and carries the highest associated mortality. There is evidence that early evacuation improves outcome.


  • 3. ASDHs usually arise from venous bleeding caused by tearing of bridging veins in the subdural space between the dura and the arachnoid.


  • 4. Surgical treatment options include burr holes, limited, or full craniotomy for evacuation of the clot.


Epidural Hematoma



  • 1. EDH is most commonly caused by arterial bleeding into the epidural space, between the skull and dura.



  • 2. Associated with temporal bone fractures causing a tear in the middle meningeal artery. Arterial blood rapidly accumulates, and patients can deteriorate quickly (so-called “talk and die”).


  • 3. Acute EDH carries 5% to 10% mortality, but emergent surgical intervention is necessary.


  • 4. Determinants of outcome include GCS score, age, presence of pupillary abnormalities, associated intracranial lesions, presence of traumatic subarachnoid hemorrhage, time between deterioration and surgery, and ICP.


  • 5. Acute EDH is seen in 1% to 10% of patients with TBI.



    • a. Nine percent of patients who are comatose after injury have an EDH requiring craniotomy.


    • b. The peak incidence of EDH occurs in the second decade of life, and it is rare after age 50.


    • c. The mean age for EDH in children is 6 to 10 years, and EDH is less frequent in very young children and neonates.


    • d. As with TBI in general, 53% (range, 30% to 73%) of EDHs are traffic-related; falls account for 30% (range, 7% to 52%) and assaults 8% (range, 1% to 19%).


    • e. Acute EDH results from injury to the middle meningeal artery (36%) or a venous structure (32%) such as the middle meningeal vein, diploic veins, or one of the venous sinuses, and this explains why the most common locations are temporoparietal or temporal lobes.


  • 6. The clinical presentation of EDH is focal deficits, hemiparesis, and decerebration. From 22% to 56% of patients are comatose on admission.



    • a. The classic “talk and die” lucid interval is seen in 47%; this is where the patient is unconscious, wakes up, and then deteriorates.



      • 1) Twelve percent to 42% remain conscious; 18% to 44% with pupillary abnormalities.


      • 2) Three percent to 27% present neurologically intact.


      • 3) Eight percent present with seizures.


  • 7. Treatment



    • a. Reasonable guidelines are that EDH should undergo urgent evacuation if GCS score is less than 9 or if there is anisocoria, or more than 30 mL of EDH; evacuation may be considered for EDH that is



      • 1) Less than 30 mL in volume, less than 15-mm thick, and less than 5 mm of midline shift, as long as the GCS score is above 8.


      • 2) These patients should undergo serial CT scanning and close observation.


Traumatic Intracerebral Hematoma



  • 1. Intraparenchymal hemorrhages (IPHs) are unusual in nonpenetrating head trauma.


  • 2. Enlarging cerebral contusions can coalesce into frank intraparenchymal clots requiring surgical intervention.


  • 3. It is more common to see IPH with penetrating injuries (i.e., gunshot and stab wounds).


  • 4. The lesion size and patient status dictate treatment.


  • 5. As with contusion, clotting factors should be checked.


Diffuse Axonal Injury



  • 1. Deceleration and rotation of the brain may result in widespread mechanical shearing of axons.


  • 2. Mortality after DAI is as high as 50%.


  • 3. DAI is the most common cause of a post-traumatic vegetative state.


  • 4. The findings of the initial CT scan are normal in 50% to 85% of patients.



  • 5. Magnetic resonance imaging (MRI) is more sensitive than CT scanning for detecting the hallmark of small punctate hemorrhages that are presumably caused by shearing of small perforating arteries.


  • 6. Many believe that lesions in the corpus callosum are a sine qua non of DAI.


Cerebral Edema



  • 1. Cerebral edema from any of the above described lesions, especially contusions, leads to increased water content and brain swelling.


  • 2. Steroids have not been effective to treat post-traumatic edema (see below).


Herniation Syndromes

May 28, 2016 | Posted by in NEUROLOGY | Comments Off on Coma, Head Trauma, and Spinal Cord Injury
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