INJURY OF THE CENTRAL NERVOUS SYSTEM
1.PRIMARY BRAIN INJURY
2.SECONDARY BRAIN INJURY
3.DELAYED POST-TRAUMATIC COMPLICATIONS
4.SPINAL CORD INJURY

INJURY OF THE CENTRAL NERVOUS SYSTEM
Primary Brain Injury
Results from what has occurred to the brain at the time of the injury
Secondary Brain Injury
Physiologic and biochemicalevents which follow the primary injury

•CEREBRAL CONCUSSION
•CEREBRAL CONTUSION
•SKULL FRACTURE
•VASCULAR AND ARACHNOID DISRUPTION
1.PRIMARY BRAIN INJURY
CEREBRAL CONCUSSION
SIGNS AND SYMPTOMS OF CONCUSSION
nUsually no head wound
nVictim may have been “knocked out” but regained consciousness quickly
nTemporary confusion
nMemory loss : anterograde (about the event) or retrograde
nBrief loss of responsiveness
nMild or moderate altered mental status
nUnusual behavior
nHeadache
A reversible physiologic change in the nervous system functions without a gross anatomic abnormalities due to transient dysfunction of the reticular systemPRIMARY BRAIN INJURY
CEREBRAL CONTUSSION
GENERAL SIGNS AND SYMPTOMS
nLump or deformity in head
nChanging levels of responsiveness
nDrowsiness
nConfusion
nDizziness
nHeadache
nClear fluid from nose or ears
nStiff neck
nUnequal pupils
nFocal sensory/motor deficits
A damage to brain parenchyma caused by head trauma producing morphological changes in brain tissue and focal neurological signsPRIMARY BRAIN INJURY
SKULL FRACTURES
CLOSED ( skin is intacted) or OPEN ( laceration overlines fracture)
hematoma within left temporal area
air inside cranial cavity
Depressed fracture of the left parietal bone associated with underlying hemorrhagic contusion and air.
DEPRESSED SKULL BONE FRACTURE
PRIMARY BRAIN INJURY
SKULL BONE FRACTURES
ANTERIOR BASAL SKULL FRACTURE
•glass-like bruises around eyes
•cerebro-spinal fluid rhinorrhea
•olfactory nerve damage
POSTERIOR BASAL SKULL FRACTURE
•bruises over mastoid process (Battle’s sign)
•cerebro-spinal fluid otorrhea
•lesion of facial and/or vestibulocochlear nerve
PRIMARY BRAIN INJURY
VASCULAR AND ARACHNOID DYSRUPTION
Vessel laceration causes secondary brain injury (intracerebral hemorrhage, hematoma, subarachnoid hemorrhage etc) while arachnoid disruption results in hygroma.
PRIMARY BRAIN INJURY
nSUBARACHNOID HEMORRHAGE
nINTRACEREBRAL HEMORRHAGE
nEPIDURAL HEMATOMA
nSUBDURAL HEMATOMA
nCAROTID-CAVERNOUS FISTULA
nSUBDURAL HYGROMA
nBRAIN EDEMA
nINFECTION
2. SECONDARY BRAIN INJURY
LAYERS OF THE MENINGES

SUBRARCHNOID AND INTRACEREBRAL HEMORRHAGES
In most cases traumatic subarachnoid hemorrhage is not so serious like in the case of aneurysm rupture and does not require special treatment.
SECONDARY BRAIN INJURY
EPIDURAL HEMATOMA
•arterial origin
•most commonly occurs in association with temporal bone fracture that transverses the middle meningeal groove where meningeal artery is situated
•clinical symptoms : -severeheadache
-lucid interval
A COLLECTION OF BLOOD SITUATTED BETWEEN SKULL AND DURASECONDARY BRAIN INJURY
SUBDURAL HEMATOMA
•venous origin
•clinical classification on the base of duration of time interval between the injury and onset of clinical symptoms : acute hematoma ( up to 24 hous)
subacute ( 1-7days)
chronic ( more then 7days)
A COLLECTION OF BLOOD SITUATTED BETWEEN DURA AND UNDERLYING BRAINSECONDARY BRAIN INJURY
CAROTID-CAVERNOUS FISTULA
CLINICAL SYMPTOMS:
•bruit synchronous with the pulse
•exophtalmos
•paralysis of the III, IV and VI cranial nerves
CAUSE: laceration of internal carotid artery as it passes through the cavernous sinus by penetrating missiles of the sphenoid boneSECONDARY BRAIN INJURY
SUBDURAL HYGROMA
Subarachnoid hygroma develops as a result of:
•cranial trauma with tearing of the arachnoid and escape of cerebro-spinal fluid
•rupture of the basal arachnoid cistern
AN EXCESSIVE COLLECTION OF CEREBRO-SPINAL FLUID IN THE SUBDURAL SPACESECONDARY BRAIN INJURY
POST-TRAUMATIC INFECTIONS
Closed head injury with skull fracture and defect in cribriform plate can give bacteria an access to the subarachnoid space.
Pneumococcusis the most common infecting organism
SECONDARY BRAIN INJURY
BRAIN EDEMA
BRAIN HERNIATIONS
•uncal invagination
•cerebellar invagination
•cingulate ( subfacial) invagination
123SECONDARY BRAIN INJURY-
-no characteristic clinical signs
-may cause ischemic stroke in area supplied by the anterior cerebral artery
1. CINGULATE HERNIATION
INVAGINATION OF THE CINGULATE GYRUS UNDER RIGID FALX OF CEREBRUMSECONDARY BRAIN INJURYSECONDARY BRAIN INJURY-CEREBRAL HERNIATIONS
CLINICAL SYMPTOMS AND SIGNS :
•initially internal then completed oculomotor nerve palsy
•hemiparesis
•infarction in area supplied by the posterior cerebral artery
2. UNCAL HERNIATION
INVAGINATION OF THE HIPOCAMPAL UNCUS UNDER THE CEREBELLAR TENTORIUMSECONDARY BRAIN INJURYSECONDARY BRAIN INJURY-CEREBRAL HERNIATIONS
CLINICAL SYMPTOMS AND SIGNS:
•bradycardia
•breath disturbances
•tetraparesis with bilateral Babinski sign
•diminishing level of consciousness
3. CEREBELLAR HERNIATION
SECONDARY BRAIN INJURYINVAGINATION OF CEREBELLAR TONSILS INTO THE GREAT FORAMEN RESULTING IN COMPRESSION OF MEDULLASECONDARY BRAIN INJURY-CEREBRAL HERNIATIONS
•EPILEPSY
•POST-TRAUMATIC ENCEPHALOPATHY
•POST-TRAUMATIC NEUROSIS
DELAYED POST-TRAUMATIC COMPLICATIONS
EPILEPSY
Classification of seizures
•immediate (at the time or within a few minutes after injury)
•early (within the first week)
•late (after the first week)
Factors influencing the likelihood of seizures:
•extent of the lesion measured by neurologic deficit
•location of the lesion (lesions around the precentral region have the highest propensity
for becoming epileptogenic)
•a presence or not infection
overallincidence of seizures in penetrating injuries = 50%DELAYED POST-TRAUMATIC COMPLICATIONS
POST-TRAUMATIC ENCEPHALOPATHY
CLINICAL SYMPTOMS :
nheadache
ndizziness
ninsomia
nirritability
ndisturbances in concentration
nanxiety
npersonality changes
Diagnostic tests ( CT, MRI or EEG) usually reveal abnormalities
DELAYED POST-TRAUMATIC COMPLICATIONSDIFFUSED BRAIN DAMAGE FOLLOWED BY HEAD TRAUMA
POST-TRAUMATIC NEUROSIS
•no correlation between severity of the injury and development of neurosis
•develops especially in patients with previously neurotic symptoms, domestic
problems or patients who desire to obtain compensation
DELAYED POST-TRAUMATIC COMPLICATIONSa syndrome of psychological origin in which the same symptoms like in post-traumatic encephalopathy are present but there are no any lesion in brain tissue and abnormalities in diagnostic tests
MECHANISMS OF THE SPINAL CORD INJURY:
PRIMARY
•compression by bone, ligaments, disk material, hematoma
•streching of tissue ( hyperflexion)
SECONDARY
•tissue edema
•circulatory disturbances
SPINAL CORD INJURY
TYPES OF VERTEBRAL COLUMN INJURIES
TEARDROP FRACTURE.
DISLOCATION
SUBLUXATION
VERTEBRAL BODY FRACTURE WITH POSTERIOR DISPLACEMENT OF BONE FRAGMENTS
SPINAL CORD INJURY
COMPLETE SPINAL CORD TRANSECTION
CLINICAL SYMPTOMS :
•motor disturbances
•sensory disturbances
•autonomic system disturbances –temperature disregulation
blood pressure disregulation
urinary bladder disfunctions
bowel disfunctions
SPINAL CORD INJURY
MOTOR DISTURBANCES
1.Spinal shock( first 3-6 weeks)
•flaccid plegia below the level of injury
•loss of reflexes as a rule but some my remain
2. Late phasegradual return or an eventual increase of reflex activity
•MASS REFLEX -contraction of abdominal muscles, triple flexion of the lower limbs, profuse perspiration, piloerection, automatic urination in response to stimulus below the lesion
COMPLETE SPINAL CORD TRANSECTION
SENSORY DISTURBANCES
1.Spinal shock-loss of all types of sensation below the level of injury
2.Late phase
•radicular pain due to nearby root involvement
•burning pains below the level of lesion
COMPLETE SPINAL CORD TRANSECTION
AUTONOMIC DISTURBANCES
1.TEMPERATURE REGULATION
•lesion above C8 -all mechanisms of termoregulation are lost
•lesion between C8 and Th 9-10 -decreasing sweating below the level of lesion
2.BLOOD PRESSURE REGULATION
•orthostatic hypotension as a result of a lack of reflex activity of the capacitance vessels in response to postural changes
COMPLETE SPINAL CORD TRANSECTION
URINARY BLADDER INNERVATION
1.VOLUNTARY ACTIVITY-(pyramidal tract)-fibers from the paracentral region of the frontal lobe innervate external sphincter and initiate/ inhibit urination
2.REFLEXIVE ACTIVITY-parasympathetic and sympathetic fibers innervate detrusor muscle and internal sphincter (smooth muscles)
BLADDER
PARASYMPATHETIC
SYMPATHETIC
FUNCTION: detrusor muscle contraction internal sphincter relaxation FUNCTION: detrusor muscle relaxation internal sphincter contraction
BLADDER DISTURBANCES
1. SPINAL SHOCK
•lack of voluntary and reflex reactivity
•marked atony and overdistention of the bladder
•overflow voiding
2.MIDDLE PHASE-symptoms of bladder disfunction depend on the level of lesion
•lesion above sacral segments
reflex bladder functions return
development of AUTOMATIC(reflex) BLADDER
•lesion at the level of conus medullarisor cauda equina
development of AUTONOMIC BLADDER( deprived of reflex activity)
voiding is never completed ( large residual volumne)
dribbling may occur
3.LATE PHASE–present only in patients with automaticbladder
Patient learns to recognize signals of bladder distention or is even able to trigger urination by such acts as abdominal pressure
COMPLETE SPINAL CORD TRANSECTION
BOWEL DISTURBANCES
1. SPINAL SHOCK
•lack of voluntary and reflex reactivity of anus sphincters
•distension and atony of bowels
•lack of peristalsis
2.LATE PHASE
•peristalsis returns
symptoms of bowel dysfunction depend on the level of lesion
lesion above sacral segments-automatic (reflex) sphincter function develops
lesion at the conus medullarisor cauda equina-sphincters deprived of any reflex activity
Reconditioning of the bowels is easier then reconditioning of the bladder

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