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Neuro Chapter 5 (139-170)
Headache
 There are no pain receptors in brain parenchyma itself; headache caused by mechanical traction, inflammation,
or irritation of other structures in head that are innervated, including blood vessels, meninges, scalp, and skull
 Supratentorial dura (most of intracranial cavity) innervated by CN V
 Dura of posterior fossa innervated mainly by CNX, but also CN IX and C1-3
 Side of headache often (not always) corresponds to side of pathology)
 Vascular headache – migraine or cluster headache; involves inflammatory, autonomic, serotonergic,
neuroendocrine, and other influences on blood vessel caliber in head
o Migraine – usually genetic basis; symptoms provoked by certain foods, stress, eye strain, menstrual
cycle, changes in sleep pattern
 Fortification scotoma – characteristic region of visual loss bordered by zigzagging lines
resembling walls of a fort
 Often unilateral, but if always on same side, MRI scan warranted to exclude vascular
malformation or other lesion as trigger
 Relief often occurs after sleeping
o Complicated migraine may be accompanied by variety of transient focal neurologic deficits (sensory
phenomena, motor deficits, visual loss, brainstem findings in basilar migraine, and impaired eye
movements in ophthalmoplegic migraine
o Acute migraine attacks usually respond to NSAIDs, anti-emetics, triptans, ergot derivatives, or other
meds and resting in dark, quiet room
 Preventative measures include beta-blockers, topiramate, valproate, calcium channel blockers,
TCAs, or NSAIDs
o Cluster headache – occur every day of over few weeks then vanish for several months; extremely severe
pain described as steady, boring sensation behind one eye; usually accompanied by unilateral
autonomic symptoms such as tearing, eye redness, Horner’s syndrome, flushing, sweating, nasal
congestion; treatment similar to migraine; inhaled oxygen helps abort attack
o Tension headache – steady dull ache described as bandlike sensation
 Chronic form associated with psychological stress
 Also seen as posttraumatic headache
 Treatment includes muscle relaxants, NSAIDs, analgesics, and TCAs
 Sudden explosive headache could be subarachnoid hemorrhage; can happen with cerebral ischemia and
infarction; low CSF pressure can occur spontaneously or following lumbar puncture resulting in headache worse
standing up and better lying down; in disorders such as neoplasms that increase intracranial pressure, headache
may be worse when lying down during night
o Headache with fever or signs of meningeal irritation, such as stiff neck and sensitivity to light, should be
evaluated for meningitis
 Idiopathic intracranial hypertension (pseudotumor cerebri) unknown cause; headache and elevated intracranial
pressure with no mass lesion; most common in adolescent females; treated with acetazolamide or shunting
procedures when severe
 Temporal arteritis (giant cell arteritis) seen most commonly in elderly; vasculitis affects temporal arteries and
other vessels, including those supplying eye
o Temporal artery characteristically enlarged and firm
o Diagnosis made by ESR and temporal artery biopsy
o Treatment with steroids essential immediately to prevent possible vision loss
Intracranial Mass Lesions
 Anything abnormal that occupies volume in cranial vault (tumor, hemorrhage, abscess, edema, etc.)
 Intracranial mass lesions cause neurologic symptoms by
o Compression and destruction of adjacent regions of brain
o Raising intracranial pressure
o Displacing nervous system structures from one compartment into another (herniation)
 Mass effect – any distortion of normal brain geometry due to mass lesion
o Effacement – mild flattening of sulci next to lesion; seen on MRI but usually asymptomatic
 Disruption of BBB results in extravasation of fluid into extracellular space, producing vasogenic edema
 Compression of ventricular system can obstruct CSF flow, producing hydrocephalus
 Lesions can provoke abnormal electrical discharges, resulting in seizures
 Large masses can produce dramatic midline shift of brain structures away from side of lesion
o Displacement and stretching of upper brainstem impairs function of reticular activating systems, causing
impaired consciousness and ultimately coma (measure this with pineal gland)
Elevated Intracranial Pressure
 Nothing in skull is compressible (though they can be deformed under pressure); whenever there is spaceoccupying or mass lesion in skull, something must leave skull to accommodate extra volume
o Smaller lesions compensated for by decrease in intracranial CSF and blood without causing much rise in
intracranial pressure
o Larger lesions overcome compensatory mechanism, and intracranial pressure rises steeply
 Severely elevated intracranial pressure can cause decreased cerebral blood flow and brain ischemia
 Cerebral perfusion pressure – mean arterial pressure minus intracranial pressure
 Autoregulation of cerebral vessel caliber can compensate for modest reductions in cerebral perfusion pressure,
leading to relatively stable cerebral blood flow
 Signs and symptoms of elevated intracranial pressure include headache, altered mental status (especially
irritability and depressed level of alertness and attention), nausea and vomiting, papilledema, visual loss,
diplopia, and Cushing’s triad (hypertension, bradycardia, and irregular respirations)
o Elevated intracranial pressure transmitted through subarachnoid space to optic nerve sheath,
obstructing axonal transport and venous return in optic nerve; papilledema takes several hours to days
to develop and often not present in acute setting
o Transient or permanent optic nerve injury can occur in association with papilledema
 Areas of decreased vision most commonly include increased blind spot or concentric visual field deficit, affecting
mainly peripheral margins of visual field
 Treatment of elevated intracranial pressure includes elevating head of bed to 30o, intubating and
hyperventilating (causes cerebral vasoconstriction), IV mannitol or hypertonic saline to increase Na+ and
osmolarity while maintaining normal volume status and BP (promotes removal of edema and other fluids from
CNS while maintaining cerebral perfusion), ventricular drainage (removal of CSF), barbiturate-induced coma
(causes cerebral vasoconstriction and reduced metabolic demands), hemicraniectomy (removal of skull
overlying mass; decompresses intracranial cavity), and steroids (reduces cerebral edema, possibly by
strengthening BBB; doesn’t improve outcome in acute head trauma, stroke, or hemorrhage)
o Goal is to keep cranial pressure low, but not so low that blood doesn’t flow
 Never lumbar puncture a patient with suspected increased intracranial pressure because of risk of herniation
Brain Herniation Syndromes
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Transtentorial (tentorial) herniation – herniation of medial temporal lobe (especially uncus) inferiorly through
tentorial notch; uncal herniation seen by clinical triad of blown pupil, hemiplegia, and coma
o
Compression of CN III, usually ipsilateral to lesion, produces first dilated, unresponsive pupil, and later
impairment of eye movements
o Compression of cerebral peduncles can cause hemiplegia; often hemiplegia contralateral to lesion either
because of uncal herniation compressing ipsilateral corticospinal tract in midbrain or because of direct
effect of lesion on ipsilateral motor cortex or both
o Sometimes midbrain pushed all the way over until it is compressed by opposite side of tentorial notch,
so contralateral corticospinal tract compressed, producing hemiplegia ipsilateral to lesion (Kernohan’s
phenomenon)
o Distortion of midbrain reticular formation leads to decreased LOC and coma
o Posterior cerebral arteries may be compressed as they pass upward through tentorial notch, resulting in
infarction
o Caused by supratentorial mass lesions
o Occasionally, large mass lesions in posterior fossa can cause upward transtentorial herniation
 Central herniation – central downward displacement of brainstem; caused by any lesion associated with
elevated intracranial pressure, including hydrocephalus or diffuse cerebral edema
o Mild central herniation causes traction on CN VI during its long course over clivus, producting lateral
rectus palsy (unilateral or bilateral)
o Larger supratentorial masses or elevated intracranial pressure can produce significant central herniation
through tentorial opening, resulting in bilateral uncal herniation
o With severe elevations in intracranial pressure, large supratentorial mass lesions, or mass lesions in
posterior fossa, central herniation can progress downward through foramen magnum
o Tonsillar herniation – herniation of cerebellar tonsils downward through foramen magnum
 Associated with compression of medulla and usually leads to respiratory arrest, BP instability
 Subfalcine herniation – unilateral mass lesions can cause cingulate gyrus and other brain structures to herniate
under falx cerebri from one side of cranium to other
o Usually no clinical signs directly attributed to this
o Sometimes one or both anterior cerebral arteries can be occluded under falx, leading to infarcts in
anterior cerebral artery territory
Head Trauma
 Concussion – reversible impairment of neurologic function for periods of minutes to hours following head injury
o Diffuse neuronal dysfunction; CT and MRI normal
o Clinical features include LOC, seeing stars, headache, dizziness, occasionally nausea/vomiting
o Occasionally anterograde or retrograde amnesia for period surrounding injury
 Postconcussive syndrome – headaches, lethargy, mental dullness, and other symptoms lasting up to several
months after accident
 Even relatively mild head injuries can occasionally cause dissection of carotid or vertebral arteries, resulting in
transient ischemic attacks or cerebral infarcts
 Diffuse axonal shear injury – causes widespread or patchy damage to white matter and CNs
 Petechial hemorrhages – small spots of blood in white matter
 Cerebral edema may occur with or without other injuries, contributing to elevated intracranial pressure
Intracranial Hemorrhage
 Classified as epidural hematoma (EDH), subdural hematoma (SDH), subarachnoid hemorrhage (SAH), or
intracerebral (intraparenchymal) hemorrhage (ICH)
 EDH – caused by rupture of middle meningeal artery due to fracture of temporal bone by head traum; rapidly
expanding hemorrhage under arterial pressure peels dura away from inner surface of skull, forming lens-shaped
biconvex hematoma that often doesn’t spread past cranial sutures where dura tightly apposed to skull
o Patient may have no symptoms (lucid interval), but within few hours, hematoma begins to compress
brain tissue, causing elevated intracranial pressure and herniation
 SDH – caused by rupture of bridging veins (particularly vulnerable to shear injury as they cross from arachnoid
into dura); venous blood dissects relatively easily between dura and arachnoid, spreading out over large area
forming crescent-shaped hematoma
o Chronic SDH – seen in elderly patients in whom atrophy allows brain to move more freely within cranial
vault, making bridging veins more susceptible to shear injury
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Venous blood collects slowly, allowing brain to accommodate and causing vague symptoms such
as headache, cognitive impairment, and unsteady gait
 Focal dysfunction of underlying cortex may result in focal neurologic deficits and occasionally
focal seizures
o Acute SDH – high velocity impact; usually associated with other serious injuries
 Typically crescent shaped and spread over large area
 Immediately, blood is hyperdense (bright on CT scan); after 1-2 weeks, begins to liquefy and
may appear isodense; if no further bleeding, after 3-4 weeks, hematoma completely liquefied
and will appear uniformly hypodense
 Sometimes with mixed-density hematomas, denser acute blood settles to bottom, giving
characteristic hematocrit effect
 Treated by surgical evacuation
SAH – blood seen on CT to track down into sulci following contours of pia
o Non-traumatic SAH – usually presents with sudden catastrophic “worst headache of my life”
 Usually occurs as result of arterial aneurysm in subarachnoid space
 Rarely happens from arteriovenous malformation
 Risk factors include atherosclerotic disease, congenital anomalies in cerebral blood vessels,
polycystic kidney disease, and CT disorders (Marfan’s)
 Saccular aneurysms (berry aneurysms) arise from arterial branch points near circle of Willis; over
85% occur in anterior circulation (carotid artery and its branches); most common locations are
anterior communicating artery (AComm), posterior communicating artery (PComm), and middle
cerebral artery (MCA)
 Can occur in branches of posterior circulation (vertebrobasilar system)
 Fusiform aneurysm – main vessel itself becoming dilated; less prone to rupture than
saccular aneurysms
 PComm aneurysm arising from internal carotid artery can cause painful third-nerve palsy
 Risk factors for aneurysmal rupture include hypertension, cigarette smoking, alcohol
consumption, and situations causing sudden elevation in BP
 Clinical effects can include headache, meningeal irritation (nuchal rigidity and photophobia), CN
and other focal neurologic deficits, impaired consciousness
 CT scan performed within first 3 days after rupture can detect hemorrhage in over 95% of cases;
important to perform CT without contrast because both subarachnoid blood and contrast
material appear white, making it difficult to see small hemorrhage
 CT better than MRI for detecting acute subarachnoid hemorrhage; after 2 days, subarachnoid
hemorrhage may no longer be visible on CT
 Lumbar puncture should be performed in suspected subarachnoid hemorrhage with negative CT
but not with positive CT because increased transmural pressure across aneurysm can
occasionally precipitate rebleeding
 Treat by clipping or coiling; choice involves shape, size, and location of aneurysm
o Following subarachnoid hemorrhage, delayed cerebral vasospasm occurs in about half of all patients
(peak severity 1 week after hemorrhage); can lead to cerebral ischemia or infarction
 Vasospasm often after triple H therapy (induced hypertension, hypervolemia, and hemodilution
in ICU); moderate hypervolemia and hemodilution usually initiated at time of hemorrhage
diagnosis in effort to prevent delayed vasospasm
 Induced hypertension done more safely after aneurysm has been clipped or coiled
 Administration of calcium channel blocker nimodipine early after hemorrhage can improve
outcome (not sure why)
 Can be treated with interventional neuroradiology procedures such as balloon angioplasty and
local injection of vasodilator papaverine
o Traumatic subarachnoid hemorrhage – caused by bleeding into CSF from damaged blood vessels
 Usually associated with severe headache due to meningeal irritation from blood in CSF
 Deficits usually related to presence of other cerebral injuries
 Vasospasm not seen
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ICH – in brain parenchyma in cerebral hemispheres, brainstem, cerebellum, or spinal cord
o Traumatic ICH – contusions occur in regions where cortical gyri abut ridges of bony skull; most common
at temporal and frontal poles; can occur on side of impact (coup injury) or side opposite impact
(contrecoup injury)
 Shearing forces can produce areas of bleeding in white matter (petechial or larger)
 When combo of ICH, SAH, and acute SDH seen on CT, head trauma can be assumed
o Non-traumatic ICH – caused by hypertension, brain tumors, secondary hemorrhage after ischemic
infarction, vascular malformations, blood coag abnormalities, infection, vessel fragility caused by
deposition of amyloid in vessel wall (amyloid angiopathy), vasculitis, mycotic (infectious) aneurysms
(endocarditis); hypertensive hemorrhage most common
 Hypertension can cause lipohyalinosis and microaneurysms of Charcot-Bouchard
(lenticulostriate arteries); most common locations are basal ganglia (usually putamen),
thalamus, cerebellum, and pons
 Can involve ventricles (intraventricular extension of ICH)
 Rebleeding rate low, although hematoma continues to enlarge
 Edema gradually develops in tissue surrounding hemorrhage
 Lobar hemorrhage – bleeding involves occipital, parietal, temporal, or frontal lobe; most
common is amyloid (congophilic) angiopathy; tend to be recurrent and multiple
 Often more superficial; can be seen in hypertension; seizures can occur preceding
hemorrhage
 Vascular malformations (arteriovenous malformations (AVMs), cavernomas, capillary
telangiectasias (capillary angiomas), and developmental venous anomalies (venous angiomas or
malformations))
 AVMS can present with seizures or migraine-like headaches in absence of hemorrhage;
usually intraparenchymal hemorrhage, but can extend to intraventricular or
subarachnoid; risk of rebleeding much lower than aneurysmal hemorrhage
 Cavernomas – abnormally dilated vascular cavities lined by only one layer of vascular
endothelium; not visible on conventional angiography; characteristic MRI appearance
o Central core of increased signal on T1 or T2 surrounded by dark rim on T2
o Patients often present with seizures
 Capillary telangiectasias – small regions of abnormally dilated capillaries that rarely give
rise to intracranial hemorrhage
Extracranial hemorrhage – hemorrhage in inner ear (hemotympanum) or subcutaneous tissues (Battle’s sign or
raccoon eyes); hemorrhage between external periosteum and galea aponeurotica can produce goose egg
(subgaleal hemorrhage); infants during delivery can have bleeding between skull and external periosteum
(cephalohematoma)
Hydrocephalus
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Caused by excess CSF production, obstruction of flow at any point in ventricles or subarachnoid space, or
decrease in reabsorption via arachnoid granulations
o Excess CSF productin usually only seen in choroid plexus papilloma
o Obstruction of CSF caused by tumors, ICH, masses, and congenital malformations; happen most often at
foramen of Monro, cerebral aqueduct, or 4th ventricle
 Obstruction can occur outside ventricles in subarachnoid space as result of debris or adhesions
from prior hemorrhage, infection, of inflammation
o Decreased CSF reabsorption at arachnoid granulations; sometimes difficult to distinguish from
obstruction
 Usually divided into communicating hydrocephalus (impaired CSF reabsorption in arachnoid granulations,
obstruction of flow in subarachnoid space, or excess CSF production) and non-communicating hydrocephalus
(obstruction of flow within ventricular system)
 Can cause CN VI palsy as well as any other signs or symptoms of increased intracranial pressure
o May compress descending white matter pathways from frontal lobe, leading to magnetic gait (feet
barely leave floor) and incontinence
 Bulging anterior fontanelle important sign of elevated intracranial pressure in infants
 When hydrocephalus more severe, inward deviation of one or both eyes may be present at rest
 In more severe or rapidly developing cases, dilation of suprapineal recess of posterior third ventricle can push
downward onto collicular plate of midbrain, producing Parinaud’s syndrome (limited vertical gaze, especially up)
o Setting sun sign – bilateral deviation of eyes downward and inward
o Abnormalities reverse after treatment
 Ventriculostomy – external ventricular drain sends fluid from lateral ventricles into bag outside head
 Ventriculoperitoneal shunt – shunt passes from lateral ventricle out of skull and into peritoneal cavity; valve
prevents reverse flow
 Endoscopic neurosurgery – narrow tube (cannula) introduced into cranium or spine through small incision and
viewing endoscope and instruments passed through cannula
o Third ventriculostomy used as alternative to shunting (make perforation in floor of third ventricle just in
front of mammillary bodies and behind pituitary infundibulum, allowing CSF to drain into
interpeduncular cistern
o Liliequist’s membrane (fold of arachnoid tissue) located in suprasellar region can revent adequate CSF
drainage if not perforated during this procedure
o Can be used to access pituitary tumors and other lesions of sellar/suprasellar region via transsphenoidal
approach
 Normal pressure hydrocephalus – characterized by chronically dilated ventricles; present with clinical triad of
gait difficulties, urinary incontinence, and mental decline
o Pressure elevations occur only intermittently
o Communicating hydrocephalus with impaired CSF reabsorption at arachnoid villi
o Patients improve after large-volume CSF removal by lumbar puncture or ventriculoperitoneal shunting
 Hydrocephalus ex vacuo – excess CSF in region where brain tissue lost as result of stroke, surgery, atrophy, etc.
Brain Tumors
 Metastases to CNS far more common than primary CNS tumors
 In adults, 70% of tumors supratentorial and 30% infratentorial; reverse is true of pediatrics
 Since pediatric brain tumors often in posterior fossa, they tend to cause hydrocephalus through compression
and obstruction of 4th ventricle or aqueduct of Sylvius
 Low-grade gliomas and meningiomas commonly associated with seizures
 Malignant brain tumors rarely undergo metastatic spread outside CNS
 Steroids often used to reduce edema
 Glioblastoma usually leads to death in 1-2 years despite maximal resection, radiation, and chemo
 Meningiomas arise from arachnoid villus cells; treated by local excision; uncommonly malignant
 Pituitary adenomas can cause endocrine disturbances or compress optic chiasm, resulting in bitemporal visual
field defect; treatment with dopaminergic agonists inhibits function and shrinks size of prolactinomas (most
common type of pituitary adenoma)
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Lymphoma arises from B lymphocytes; common involves regions adjacent to ventricles (diagnosed by CSF
cytology); HIV infection increases risk; controlled with chemo and radiation (median survival rate 4 years)
 Pineal region tumors (pinealomas, germinoma, teratoma, glioma) may obstruct cerebral aqueduct, causing
hydrocephalus; may compress dorsal midbrain, causing Parinaud’s syndrome
 Lung carcinoma, breast carcinoma, and melanoma can metastasize to brain
o Most common tumor causing brain hemorrhage is lung cancer
 Paraneoplastic syndromes – neurologic disorders caused by remote effects of cancer in body, leading to
abnormal autoimmune response
o Tumors that most often cause these include small cell lung carcinoma, breast cancer, and ovarian cancer
o Testing for specific antibodies that cross-react with tumor cells may be helpful in diagnosis
Infectious Disorders of the Nervous System
 Bacteria most often gain access to nervous system through bloodstream, frequently originate from infection
elsewhere in body, such as respiratory tract or heart valves (endocarditis)
o Can spread by direct extension from oronasal passages
 Infectious meningitis – infection of CSF caused by bacteria, viruses, fungi, or parasites
o Kernig’s sign – pain in hamstrings when knees straightened with hips flexed
o Brudzinski’s sign – flexion at neck causes hips to flex
o Nuchal rigidity – neck muscles contract involuntarily, resulting in resistance to active or passive neck
flexion, accompanied by neck pain
o Diagnosis made by lumbar puncture; head CT should always be performed first to rule out presence of
mass lesion that would precipitate herniation if lumbar puncture performed
o Bacterial meningitis – usually treat with ampicillin and ceftriaxone (depends on age and pathogen)
 CSF will have high WBC, high polymorphonuclear predominance, high protein, low glucose
 Begin treatment rapidly because patients can deteriorate rapidly
 Screen children for hearing loss after they get better; can be treated early by cochlear implant
 Brain abscess – expanding intracranial mass lesion caused by bacterial infection; presents with headache,
lethargy, fever, nuchal rigidity, seizures, nausea/vomiting
o ESR usually elevated; more than one organism often present
o Small abscesses treated with antibiotics and careful observation
o Patients with larger abscesses at risk for rupture or with clinical signs of mass effect should be treated
with sterotactic needle aspiration or surgical removal with antibiotics
 Epidural abscess – happens often in spinal canal; presents with back pain, headache, signs of nerve root or spinal
cord compression, fever, high WBC count
o Treated with surgical drainage and antibiotics (nafcillin and ceftriaxone)
 Subdural epyema – collection of pus in subdural space, usually resulting from direct extension from infection of
nasal sinuses or inner ear
o Treated by urgent surgical drainage and antibiotics (ceftriaxone plus metronidazole)
 Tuberculous meningitis – meningitis symptoms; inflammatory response in basal cisterns of brain, can affect
circle of Willis vessels, resulting in infarcts
o Pott’s disease – tuberculous involvement of epidural space and vertebral bones
o Meningeal involvement results from reactivation of previous TB infection; CSF has lymphocyte
predominance, elevated protein, and low glucose
 Lymphocyte-predominant meningitis (aseptic meningitis) caused by TB, cat scratch disease (headaches, mental
status change, and seizures); MRI may show T2 bright areas; CSF either normal or shows lymphocytepredominant meningitis
 Neurosyphilis – tertiary syphilis infection; can cause aseptic meningitis, sometimes associated with CN II, VII, or
VIII palsy; can follow 4-15 years latency
o Meningovascular syphilis – chronic meningeal involvement causes arteritis in medium-sized vessels
o General paresis – accumulation of lesions causes dementia, behavioral changes, delusions of grandeur,
psychosis, and diffuse UMN-type weakness
o Tabes dorsalis – involvement of spinal cord dorsal roots, resulting in degeneration of dorsal columns
o RPR or VDRL may be positive or negative in neurosyphilis; CSF VDRL usually positive
o Treated with IV penicillin G
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Lyme disease – erythema chronicum migrans (initial raised rash); gradually shifts location and enlarges over days
to weeks; neurologic manifestations can occur (meningeal signs and emotional changes, impaired memory)
 Viral meningitis – usually recover in 1-2 weeks spontaneously; same symptoms as bacterial meningitis
o CSF shows elevated WBC count, normal or mildly elevated protein, normal glucose
o Type of aseptic meningitis
 Viral encephalitis – viral infection involving brain parenchyma; meningoencephalitis if meninges involved
o Most commonly caused by herpes type 1; has trophism for limbic cortex
o Patients present with bizarre psychotic behavior, confusion, lethargy, seizure, meningitis symptoms
o Causes necrosis of unilateral or bilateral temporal and frontal structures often visible on MRI
o Treat promptly with acyclovir
o CSF has lymphocytic predominance, elevated protein, normal glucose; when necrosis prominent, RBC
count elevated and glucose decreased
 Postinfectious encephalitis – diffuse autoimmune demyelination of CNS several days after viral infection
 Subacute sclerosing panencephalitis – measles can cause this; progressive fatal encephalitis
 Herpes zoster (chicken pox or shingles) causes painful rash conforming to nerve root distributions
 Transverse myelitis – caused by viral infections of nervous system
 HIV-associated neurocognitive disorder (HAND) – treatment with antiretroviral agents can cause some
improvement in AIDS-related dementia
o Associated with myelopathy (spinal cord), neuropathy (peripheral nerves), and myopathy
o CMV can cause retinitis
o Cryptococcal meningitis should be suspected in all HIV patients with chronic headache (fungal)
o Toxoplasmosis – caused by reactivation of infection with parasite from undercooked meat or cat feces;
usually asymptomatic at initial infection; forms brain abscesses seen as ring-enhancing lesions on MRI
 Most common cause of intracranial mass lesions in patients with HIV
o Increased risk for primary central nervous system lymphoma
 Cysticercosis – caused by ingestion of eggs of pork tapeworm; worm migrates through bloodstream and forms
cysts in muscles, eyes, and CNS; seizures common; can cause headache, nausea, vomiting, lymphocytic
meningitis, and focal deficits; spinal cord occasionally involved
o Organisms eventually die, leaving calcifications scattered throughout brain (brain sand)
 Fungal infections of CNS uncommon in immunocompetent hosts
o Mucormycosis occurs mainly in diabetics in rhinocerebral form and involves orbital apex; maybe fatal
 Causes ophthalmoplegia, facial numbness, visual loss, and facial weakness; typical violet
coloration of tips of eyelids
o Steroids can exacerbate fungal infections and should be avoided when fungal infection suspected
 Creutzfeldt-Jakob disease – rapidly progressive dementia, exaggerated startle response, myoclonus, visual
distortions or hallucinations, and ataxia; EEG shows periodic sharp wave complexes, especially late in illness
o CSF shows increased 14-3-3 protein
o MRI shows increased signal in basal ganglia and cortical ribbon on diffusion weighted imaging (DWI)
o Death in 6-12 months; no treatment
Lumbar Puncture
 Caution should be used in cases of impaired coagulation because of risk of iatrogenic spinal epidural hematoma,
which can compress cauda equina
 May be done with patient lying or seated; pressure measurements more reliable in lying position
 Conus medullaris ends around L1-L2, so usually use L4-L5 vertebral space
 Order tubes are drawn can effect cell count
 Traumatic tap – introduction of RBCs to subarachnoid space during tap
o Number of RBCs usually decreases from first to last tubes of CSF collected in traumatic tap, but not
subarachnoid hemorrhage
o If CSF centrifuged, supernatant may have yellowish (xanthochromic) appearance as result of RBC lysis if
hemorrhage occurred several hours previously, but not in traumatic tap
o Ratio of RBCs to WBCs can help determine what WBCs were introduced by traumatic tap
Craniotomy
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Burr holes drilled through skull at several locations in operative field; care taken not to enter dura; burr holes
joined by small saw so bone flap can be removed, exposing dura
Lumbar drain sometimes used to remove controlled amounts of CSF and enhance mechanical brain relaxation
Pterional craniotomy – provides access to inferior frontotemporal lobes; used for surgery on anterior circulation
and basilar tip aneurysms, cavernous sinus, and suprasellar tumors
Sterotactic procedures – instrument introduced through burr hole and directed to specific target deep in brain
Neuroendoscopic procedures to reach intraventricular structures through right lateral ventricle and foramen of
Monro; transsphenoidal approach used for sellar and suprasellar regions