CNS TRAUMACNS TRAUMA

DR Anwar Wardy W, dr.SpS, DFMFebruary 2012

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TRAUMATRAUMA• Concussion • Cerebral contusion • Epidural hematoma • Subdural hematoma/effusion • Intracerebral hematoma• Diffuse axonal injury

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EPIDURAL HEMATOMAEPIDURAL HEMATOMA

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SUBDURAL HEMATOMASUBDURAL HEMATOMA

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DD:Metabolic DD:Metabolic Disorders Disorders

• Hypoglycemia • Acidosis • Hyperammonemia• Uremia

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General Physical ExamGeneral Physical Exam• Vital signs oTemperature -fever (may mean infection) oVery high temperature and dry skin –

consider heat stroke oHypothermia often seen in drug

intoxication

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• Pupillary response

o pupillary constriction is controlled by the parasympathetic system in the third nerve

oDilation mediated by the sympathetic system –hypothalamus to spinal cord and then the superior cervical ganglia

NEUROLOGIC EXAM

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Cranial Nerve Exam Cranial Nerve Exam • I. olfactory-smell• II. Optic-Visual acuity, visual fields, • III. Oculomotor - eye movement • IV. Trochlear eye movement • V. Trigeminal Nerve - facial sensation, corneals, • VI. Abducens-eye movement • VII. Facial nerve - motor and sensory to face • VIII. Acoustic nerve - hearing• IX. Glossopharyngeal - gag reflex, elevate palate • X. Vagus - swallowing movement of the cords • XI. Accessory Nerve - sternocleidomastoid muscle , trapezius

function • XII. Hypoglossal nerve - tongue movement, fasciculations

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Corneal reflex Corneal reflex • Test the fifth nerve sensory and seventh

nerve motor• Cotton on cornea and look for a blink or

watch the lower eyelashes move toward the midline

• Good test for mid and low pontine dysfunction

• Swab the nose to test seventh nerve

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Respiratory Respiratory Pattern Pattern

• Injury location and type of breathing o Post hyperventilation apnea -bilateral

hemispheric dysfunction • Cheyne-stokes breathing

o Central reflex hyperpnea- bilateral hemispheric dysfunction injury to lower midbrain or upper pons

o Apneustic respiration- ponso Central Neurogenic Hyperventilation (formerly

known as Ondine’s curse) loss of involuntary respiration- medulla

o Apnea-medulla to C4, neuromuscular junction

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UPPER MOTOR NEURON UPPER MOTOR NEURON LESIONSLESIONS

• Cerebrum oAphasia cortical sensory loss oGaze preference oNystagmusoVisual field deficit

• Internal capsuleo Equal paralysis of arm, legs, face oMotor loss without sensory loss oMotor loss with dense hemi sensory loss

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UPPER MOTOR NEURON UPPER MOTOR NEURON LESIONSLESIONS

• Midbrain-hemiplegia with contralateral 3rd nerve palsy-Weber’s

• Pons-Hemiplegia with contralateral 6th or 7th palsy-Millard Gubler

• Medulla-spastic weakness difficulty swallowing

• Spinal cord -weakness of one with contralateral loss of pain – Brown-Sequard /or paraplegia

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INFRATENTORIAL INFRATENTORIAL LESIONSLESIONS

• Brainstem symptoms are often seen initially

• Sudden onset of coma • Cranial nerve abnormalities • Alteration of the respiratory

pattern

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The The ABCDEsABCDEs of trauma care sequentially of trauma care sequentially identify life-threatening conditions identify life-threatening conditions A. A. AirwayAirway maintenance with cervical maintenance with cervical spine spine protection protection B. B. BreathingBreathing and ventilation and ventilation C. C. CirculationCirculation with hemorrhage control with hemorrhage control

D. D. DisabilityDisability: Neurologic status: Neurologic status E. E. ExposureExposure: Completely undress but : Completely undress but prevent hypothermia prevent hypothermia Life-threatening conditions are identified Life-threatening conditions are identified and and simultaneous management is instituted simultaneous management is instituted

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KEY TO DIAGNOSIS KEY TO DIAGNOSIS

• A good history • A thorough physical exam • Knowledge of CNS anatomy

Neurologic EvaluationNeurologic EvaluationLevel of consciousnessLevel of consciousness

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AVPU method: A - Alert, V - Responds to Vocal stimuli P - Responds only to Painful stimuli U - Unresponsive to all stimuli Pupillary size and reaction.

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Pupillary response Pupillary response • Mid-position unreactive pupils

o both parasympathetic and sympathetic mid brain lesions

• Pinpoint pupils –parasympathetic innervation is intact but sympathetic nerve is involved-pontine lesions

• Unilateral dilation –uncal herniation from compression of oculomotor nerve

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Pupillary reflex Pupillary reflex • Metabolic causes of coma

oCan give a variety of changes but pupils usually remain reactive

• Drugs: oNarcotics-pinpoint but reactive oAtropine-dilated and nonreactive

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Glasgow Coma Scale Glasgow Coma Scale • Developed to define outcome in adult

patients with head injury • Coma: score of 8 or less• There is a modified scale used for

infants and children

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Glasgow Score Glasgow Score • Eye opening Motor Response

o Spontaneous 4 obeys commands 6o To command 3 localizes pain 5o To pain 2 withdraws to pain 4o None 1 abnormal flexion 3

• Verbal abnormal extension 2o Oriented 5 none 1o Confused 4o Inappropriate words 3 TOTAL 3-15o Incomprehensible sounds 2o None 1

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MODIFIED GLASGOW MODIFIED GLASGOW COMA SCORE For COMA SCORE For

Infants Infants • Eye opening Motor

o spontaneous 4 normal 6o To speech 3 withdraws to touch 5o To pain 2 withdraws to pain 4o None 1 abnormal flexion 3

• Verbal abnormal extension 2o Coos 4 none 1o Irritable cries 4o Cries to pain 3o Moans to pain 2o None 1

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Glasgow Coma Glasgow Coma ScaleScale

A strong predictor of outcome13: mild brain injury9-12: Moderate brain injury< 8: Severe brain injury (coma)

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Progression of Mass LesionsProgression of Mass Lesions

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Herniation Herniation

Skull FractureSkull Fracture• This is a simple,

single line fracture that has reached the posterior midline suture to open it.

• There is an epidural hematoma in the occipital region at the site of impact.

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Middle Meningeal Middle Meningeal ArteryArtery

• This is a display of a young (straight) middle meningeal artery serving the dura.

• Pressure in the artery creates a canal on the inner table of the skull.

• A fracture with shifting bone plates severs the artery for instantaneous bleeding and rapid expansion.

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Epidural HematomaEpidural HematomaThis hematoma is seen to be between the dura and skull.

• The dura ordinarily would be tight and tamponade (stop) the bleeding.

• The fracture loosened the dura to allow easy and fatal expansion against a soft brain.

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Cerebral EdemaCerebral Edema• Swelling of tissue

can become severe to flatten gyri against the skull.

• Sulci are obliterated and major arteries traversing the sulci get compressed, congested, and may thrombose.

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Compression by Compression by HematomasHematomas

• Both epidural and subdural hematomas become space occupying and brain-deforming phenomena.

• All gyri are flattened and vessels congested.

• The hemisphere can only go under the falx, down to the posterior fossa (uncal herniation) and out the foramen magnum (tonsillar herniation.)

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Cerebral ContusionsCerebral Contusions• Though from another

patient, the temporal contusions are similar

• Bleeding into the cingular gyrus is likely from hitting the falx.

• In this case, contusions are seen in the opposite temporal lobe as well.

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Radical Surgical Radical Surgical DecompressionDecompression

• When cerebral edema is severe, one or both sides of the skull can be surgically removed while leaving a midline basket handle for later adhesion.

• Our patient had one side fractured so it was stored for later.

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Reactions at the Reactions at the Cellular LevelCellular Level

• While all cells in the center of the injury may die, those at the edge can show reversible forms of injury.

• This is an axonal torpedo formed by cytoplasmic jamming at a node of Ranvier.

• The silver is staining neurotubules, fibrils, mitochondria, and endoplasmic reticulum.

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Uncal HerniationUncal Herniation• Unilateral edema can

push the uncus of the temporal lobe into the posterior fossa (arrow).

• This can compress the posterior cerebral artery against the midbrain for an occipital infarct.

• It can also push the midbrain against the opposite tentorium to create Kernohan’s notch and ipsilateral hemiplegia

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Tonsillar HerniationTonsillar Herniation• The arrows point to

bilateral cerebellar tonsils formed under pressure from edema above.

• You can approximate the size of the foramen magnum by the tonsils.

• Compression of the basilar artery is a potential fatal complication.

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Acute Duret Acute Duret HemorrhagesHemorrhages

• Had the temporal lobe not been removed, the pons would have been pushed away from the basilar artery for infarction followed by hemorrhages.

• Not how swollen, round, and pale the pons has become.

• The midline ventral trench for the basilar artery no longer suffices!

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Chronic Duret Chronic Duret HemorrhageHemorrhage

• This patient somehow survived one year after his secondary Duret hemorrhages.

• Note they still contain hemosiderin stains along the lining of the cavities.

• The aqueduct shows “hydrocephalus ex vacuo.”

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Old ContusionOld Contusion• The margin of temporal lobe dissection and the injured gyri have lost their edema and most tissue, but still have hemosiderin macrophages providing a green hue like a bruise.• Neighboring gray matter may be intact a short segment before another injured spot (on the right). These islands can cause seizures if axons survived.

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Resolving ContusionResolving Contusion• While most dead

tissue is gone, some hemosiderin-laden macrophages have yet to return to the vessels.

• No tissue remains under the arachnoid on the right (strokes leave layer I).

• Surviving vessels are condensed and markedly thickened.

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Critical SitesCritical Sites• A basal skull fracture

can lead to bleeding and adhesions over the foramina of Magendie and Luschka and then hydrocephalus.

• The nucleus basalis of Meynert and hippocampus can be damaged to cause traumatic Alzheimer’s disease, as in this patient.

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Traumatic AlzheimerTraumatic Alzheimer’’ss• Veterans and

athletes with head injuries have a higher incidence of senile plaques and tangles.

• They can be “punch drunk” while young and demented early as an older adult.

• The same applies to auto accident victims.

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15 vs 100 Year Old Brains 15 vs 100 Year Old Brains Note the open sulci and Note the open sulci and

ventricles.ventricles.

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REFERENCESREFERENCES• Robbins, 7th ed, 2005:1356-61• Townsend J, Klatt EC. Neuropathology Illustrated,

Dept Pathology, Univ Utah, Salt Lake, 2001• McArthur DL, Hovda DA. Symposium – Traumatic

Brain Injury. Brain Pathology 2004;14:183-222• Whitelaw A, Love S. Symposium – Hydrocephalus

(especially post-traumatic). Brain Pathology 2004;14:304-36

• Jones NC et al. A detrimental role for nitric oxide synthase-2 in the pathology resulting from acute cerebral injury. J Neuropath Exp Neurol 2004;63:708-20

• All illustrations are from the first two references.

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Wassalam,….Terima Wassalam,….Terima kasihkasih

DR Anwar Wardy W, dr.SpS, DFM(K)Email: anwarwardy@gmail.comAnwar_wardy@yahoo.comBlog’s and fb: anWARdy…neurovision…//

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