Neuro Clin Med

Patho/etiology of trigeminal neuralgia

• CN V: supplies sensation to face, sensory/motor function for muscles of mastication

• 3 major divisions of CN V: ophthalmic (V1), Maxillary (V2), Mandibular (V3)

• MC in middle aged women

• compression of the trigeminal nerve root (by the SCA or tortuous vein (90%) or idiopathic)

• also caused by MS or secondary (central pain syndrome)

• mainly in V2 or V3 division

signs/symptoms of trigeminal neuralgia

• unilateral pain at maximum onset

• lightning-like pain by innocuous stimulus (chewing, smiling, ex)

• MC: arise near side of mouth: shoots to ear, eye, nose

• lacrimation, conjunctival injection, rhinorrhea

diagnosis for trigeminal neuralgia

• MC: pt History

criteria for dx:

1. at least 3 attacks of unilateral pain in 1+ divisions

2. no clinical neurologic deficit

3. no other cause for pain

pain with 3 out of 4 characteristics:

1. recurrent plus lasts 4 sec to 2 min

2. severe

3. shock-like, shooting, stabbing, or sharp

4. 3+ attacks by innocuous stimuli

• brain MRI to help distinguish structural abnormalities

if found in person <40 years, can be MS

Treatment for trigeminal neuralgia

1st line

• oxcarbazepine or Carbamazepine (check CBC for potential leukopenia)

2nd line (add)

• baclofen + gabapentin

do surgical decompression if:

• microvascular compression

• pts with MS + secondary HTN

• tumors

patho/etiology of Bell’s Palsy

• acute idiopathic palsy of facial nerve (CN VII)

• cause: reactivation of dormant HSV

residing within geniculate ganglion

• reactivation results in facial paralysis by inflammation plus demyelination of peripheral nerves

MC: pregnancy + diabetes

DDX: stroke (does not cause these sx as Bell’s is on whole face where stroke spares forehead)

signs + symptoms of Bell’s Palsy

• abrupt, unilateral facial paralysis

• pt unable to close eye on affected side ( CN III open and CN VII close)

• facial droop, sagging eyebrow, and droop corner of the mouth

• disturbance of taste (ant 2/3 of tongue), hyperacusis (hypersensitive to sound)

Diagnosis of Bell’s Palsy

• based on pt presentation by ruling out other causes like stroke

  • paralysis must affect distribution of CN VII, including eyebrows and forehead (inability to raise eyebrow= Bell’s)

• resolution within 6 months

Treatment of Bell’s Palsy

• 60% recover without treatment

• with treatment:

  • start 3 days within onset

  • steroids (60 mg then taper)

  • combo of glucocorticoids + antivirals (valacylovir + acyclovir)

  • eye protection + artificial tears

patho/etiology of post herpetic neuralgia

• HZV outbreaks happen in other dermatomes, but MC is trigeminal nerve distributions (15% of pts)

• 3 phases of pain with HZV

  • acute: pain preceding/accompanying rash; </= 30 days)

  • subacute: pain after rash gone, lasts < 4 months

  • post-herpetic: pain >/= 4 months

• MC: elderly or immunocompromised (severe rash, 1st division of CN V)

• Hutchinson sx (vesicles on top of the nose with issues with ophthalmic CN)

• Ramsay-Hunt (HZV affect external ear canal)

signs + symptoms of Post-Herpetic Neuralgia

• continuation of pain experienced with acute pain

• develop months to years after initial attack

• burning, pruritis, stabbing, constant, OR intermittent pain

• Allodynia: increased sensitivity to touch

• sensory changed in affected dermatome

treatment for post herpetic neuralgia + prevention

• 1st line

  • Gabapentin or Pregabalin (SE: drowsiness)

• tricyclic antidepressants (TCAs)

  • amitriptyline: cause sedation

• prevention

  • treat acute rash with antiviral (acyclovir or valacyclovir)

  • zoster vaccine to pts > 60 years

patho/etiology of glossopharyngeal neuralgia + signs/sx

patho

• uncommon

• involves 9th and 10th CNs (glossopharyngeal + vagus)

signs/sx

• paraoxysmal, intense pain in tonsillar fossa of throat from swallowing

• shooting, severe pain like trigeminal neuralgia

• pain in tonsillar fossa, throat, ear/back of tongue

• precipitated with swallowing, chewing, etc.

• ± associated syncope

treatment of glossopharyngeal neuralgia

• similar to trigeminal neuralgia

• #1: oxcarbazepine + carbamazepine

• surgery for those refractory to meds

signs +symptoms of atypical facial pain

• pain without features of trigeminal neuralgia

• constant, burning pain that spreads to rest of the affected side

• can involve other side of head, back, and neck

• MC: middle-aged woman who are depressed

treatment for atypical facial pain

• simple analgesics, TCAs, -zepines, phenytoin

• No surgical attempts

How to distinguish atypical facial pain from other “facial pain” diagnosis?

• pain without typical features; constant

• burning usually in one area @ onset & then spreads to rest of face

• sometimes spread to another side of face to even back of the head

• often in middle aged women with depression

DDX of trigeminal neuralgia vs. HZV vs. glossopharyngeal neuralgia

Trigeminal neuralgia

• Pain: acute, shooting, severe, unilateral

• causes/precipitating factors: compression of CNS, MS, central pain syndrome

• Tx: anti-seizure meds (-zepine), surgery if refractory

herpes zoster

• pain: preceded or coms with rash or blisters

• causes: immunocompromised

• tx: acyclovir/valacyclovir

glossopharyngeal neuralgia

• pain: shooting severe in throat, tonsillar fossa, ear, back of the tongue

• causes: talking, swallowing, chewing, yawning

• tx: antiseizure med (-zepine), surgery if refractory

definition of transient ischemic attack (TIA)

• brief neurological dysfunction due to interruption of blood supply to the brain/eye

• without infarction lasting < 24 hrs (usually < 30 min)

• usually focal

• warning sign: atherosclerosis of vessel

patho/etiology of TIA

Patho

• MCC: emboli entering carotid or vertebrobasilar system (arthrosclerosis)

• causes focal ischemic cerebral neurologic deficits

• RF: age + HTN (atherosclerosis) and afib

hematologic causes

• GCA, polyarteritis, anemia, polycythemia

signs + symptoms of TIA

• Neurologic deficits lasting <24hrs depending on artery (rapid recovery); ± stroke-like sx (slurred speech)

• carotid bruit (turbulent flow heard)

• amaurosis fugax (transient mononuclear vision loss)

• rare sx (LOC/confusion)

  • depends on arterial distribution

stroke risk

• RISKS

  • >60 years, DM, TIA, >10 min

Diagnosis of TIA

• CT without contrast/MRI to rule out bleed

• follow with CTA (vessels + circulation)

• MRI to have location and size

• carotid U/S to see carotid stenosis or hear bruits

• rule out hypoglycemia

• monitor for arrhythmias

treatment for TIA

• aimed to prevent future attacks

• smoking cessation, control HTN, DM, hyperlipidemia

• antiplatelet meds

  • ASA 1st in acute phase

  • secondary is adding clopidogrel/dipyridamole

• carotid stenosis: carotid endarterectomy

• HTN control unless BP > 220/120 mmHg

• anticoag for afib with warfarin after discharge

• at home: Aspirin + statin (to lower lipid)

what is amaurosis fugax?

• embolism from ipsilateral carotid of heart lodged in retinal circulation

• visual loss in one eye with curtain down

• tx: antiplatelet agent

what is ABCD2 scoring?

• utilize to estimate the risk of stroke

• Age >/= 60 yrs: 1 pt

• Blood pressure >/= 140/90 mmHg @ initial eval: 1 pt

• Clinical features of TIA (unilateral weakness): 2 pts

• Speech disturbance: 1 pt

• Duration of sx (10-59 min): 1 pt; >/=60 min: 2 pt

• Diabetes mellitus, 1 pt

hospitalization of score 3+ to expedite workup

Risk Factors: Ischemic vs Hemorrhagic stroke

Ischemic stroke

• thrombotic (MC) + embolic

• Afib, atherosclerosis

• HTN (MCC)

• male, age, family hx

Hemorrhagic stroke

• aneurysms, smoking, HTN

• bleeding into brain

Patho/Etiology of ischemic stroke

• more likely in AA (2x)

• brain neurons damaged by reduce blood flow + O2

causes

• thrombosis due to atherosclerosis

• embolization: migration of clot

• low perfusion (like arterial dissection)

the lobes of the brain

• frontal lobe: control of movement, frontal eyelids, control speech, memory + personality

• parietal lobe: sensory cortex (integration of sensation)

• temporal lobe: receptive language (Wernicke) + memory processing

• occipital lobe: visual cortex

signs and symptoms of cortical stroke

anterior cerebral artery (ACA)

• weakness + cortical sensory loss in contralateral leg

• urinary incontinence, gait apraxia, aphasia

• frontal lobe affected

Middle cerebral artery (MCA): most common

• contralateral face + arm weakness and/or sensory deficit

• aphasia (expressive: Brocca) + receptive (Wernicke)

• affects frontal, parietal, and temporal lobes

Posterior cerebral artery (PCA)

• homonymous hemanopia

• affects occipital and temporal

• alexia (inability to read)

• contralateral loss of pain + temp sensation

signs and symptoms of Lacunar Infarction

• small lesions that occur in distribution of short penetrating arterioles in anything below brain stem

• pure motor hemiparesis of face, arm, leg

• dysarthria (clumsy hand)

• vascular dementia

signs and symptoms of cerebellar stroke

• ipsilateral limb ataxia (lack of coordination)

• vertigo

• wide-based imbalance

• nystagmus, nausea + vomiting

• intentional tremor

what is NIH stroke scale?

• quantitative measure of stroke-related

• utilized to see TPA eligibility

• within 3-4.5 hrs

Score

• 0: none

• 1-4: minor stroke

• 5-15: moderate stroke

• 16-20: moderate-severe

• 21-42: severe stroke

TPA for 5-24

no TPA with >25

diagnostic of ischemic stroke

• Head CT w/out Contrast : r/o bleed

• CT scan w/ CTA to provide detailed images of arteries in brain + neck

• MRI to identify infarcts earlier than CT (not always available in timely manner)

• ESR, sugar test, INR, PT/INR

• ECG: a-fib (embolic)

blood pressure management for Penumbra from ischemic stroke

• Penumbra is inflamed brain tissue after stroke

• keep BP high to preserve penumbra

  • no lowering in first 24 hours unless > 220/120 mmHg

  • TPA: <185 systolic, <110 diastolic (give small doses of BP meds)

• brain needs perfusion

eligibility for TPA

• last seen normal for TPA <3-4.5 hrs

• Age >18

• deficit on NIHSS <25

• baseline CT with no intracranial hemorrhage

• INR <1.7

Exclusion for TPA

• BP >185 mmHg + >110 mmHg(lower)

• ischemic stroke within 3 months

• MI within 3 months

• GI or GU hemorrhage within 21 days

• major surgery within 14 days

• INR >1.7, PT> 15 sec

• rapidly improve sx (more like TIA)

• platelet <100,000

• glucose <50 mg/dL or > 400 mg/dL

• age >80

• NIHSS >25

Treatment for ischemic strok

• antiplatelet therapy: ASA + clopidogrel(Plavix)/dipyridamole

• 21-90 days of single platelet

• TPA give ASA 325 mg 24 hrs post IV TPA

• later, 81 mg of ASA daily at home

• allergy to ASA: use Plavix

• exercise → weight loss

• HTN meds

• DM management

signs and sx , dx, and tx of embolic stroke

• afib, contralateral hemiparesis + sensory loss

• apraxia + aphasia

Dx

• non contrast CT

• carotid U/S

• EKG (for afib)

Tx

• antiplatelet therapy

• anticoag (warfarin) and stop ASA tx

• smoking cessation

Types of Hemorrhagic Strokes

intracerebral hemorrhage

• 70-75%

• bleeding from blood vessels within brain

subarachnoid hemorrhage (25%)

• bleeding in subarachnoid space (between brain and membrane)

Vascular Malformations (1-2%)

• tangle of blood vessels

• irregularly connect arteries plus veins, disrupting blood flow + O2 circulation

patho/etiology of hemorrhagic stroke

• presents with headache + rapid deterioration in level of consciousness

• vomiting and drowsiness occur as ICP increases

• leading cause: HTN

• HTN hemorrhages classically occur in subcortical structures

  • basal ganglia, thalamus

  • cerebellum, Pons (Part of brainstem)

signs + sx of hemorrhagic stroke

• depend on where bleed is

• blood irritating the CSF

• HA, N/V, nuchal rigidity

• increased ICP

  • worsen brain ischemia

  • HA, N/V, lethargy, change in consciousness

• Cushing Reflex (HTN, bradycardia, irregular respirations)

• ipsilateral fixed dilated pupil with contralateral hemiparesis

types of hydrocephalus

• increased CSF volume with increased ICP plus cause dilation of ventricles

communicating: no obstruction to ventricular flow

• decrease absorption of CSF

• causes: meningitis, SA hemorrhage, CSF reabsorption

• normal pressure hydrocephalus

noncommunicating

• caused by structural blockage of CSF

• circulation within ventricular system

• occur from stenosis (narrow), tumor, or colloid cyst

Dx of Hemorrhagic Stroke

• CT w/out contrast: confirm + locate size + site of bleed

• MRI to see vessels better

• CTA for aneurysm

• enhanced MRI for those without hx of HTN

  • r/o cerebral amyloid or CA malformation

• CBC, platelet, PT, PTT, CMP

• LP can detect blood or infection of CSF

  • may precipitate herniation syndrome

treatment/management of hemorrhagic stroke

• admit to ICU

• ventriculostomy

• elevate head to reduce ICP

• drain CSF via ventriculostomy

• osmotherapy: Mannitol

• hypothermia to 33 C

• glucocorticoids: dexamethasone 4 mg

• begin anti-seizure meds: consider EEG

• decompressive craniectomy

• systolic BP lowered to <140-160 mmHg

• platelet transfusion

pathology/etiology of mild traumatic brain injury (concussion)

• alteration in mental status caused by trauma, with or without loss of consciousness due to sports, etc.

• can have brain confusion (bruising of brain tissue from direct tract and croup (front) or contrcap (opposite)

• persistent + progressive decline in level of consciousness

signs + sx of mild traumatic brain injury (concussion)

• alert followed by a brief period of unconsciousness

• HA, nausea, confusion, disorientation

• dizzy, imbalance, emesis (vomit)

• brief amnesia

• photophobia, irritable, phonophobia

diagnosis of mild TBI (concussion)

head CT: CGS <15

• Seizure

• age 65+

• focal neurodeficit

• skull fracture

• HA + vomit

• intoxication

• C spine radiograph

• Pts needing CT admit unless

  • CT normal

  • GCS= 15

  • No seizures or bleeding

  • monitored by caregiver

treatment and prevention for mild TBI (concussion)

• rest at least 24 hours

• gradual return

prevention

• helmet, seatbelt, safety

complications of mild TBI (concussion)

post-conductive syndrome

• HA ,dizzy, fatigue, noise sensitive, sx for weeks to months

• MRI

• tx: manage sx, cognitive behavior sx

second impact syndrome

• recurrent concuss while pt symptomatic from first

• lead to fatal cerebral edema

chronic traumatic encephalopathy

• repeat concussions causing cumulative neuropsych def.

• personality changes, cog impairment, speech + gait abnorm

patho/etiology for moderate to severe TBI

• elevated ICP resulting from diffuse axonal injury or hematoma or etc.

• pts need to be hospitalized

• cognitive impairment in temporal + frontal lobe affecting attention, memory, judgment, and executive function

signs + sx of moderate to severe TBI

• behavioral dysregulation, depression, disinhibition

• anosmia (decreased smell)

• GCS score of </= 8

diagnosis of moderate to severe TBI

• CT + MRI for bleeding + skull fracture

• GCS: <8 = 30% survival rate

• less likely for severe disability

  • 1. follow commands is <2 weeks

  • 2. duration of post-traumatic amnesia <2 months

• unlikely to have good recovery

  • time to follow command>1 month

  • duration of post-trauma amnesia > 3 months

  • Age >65

treatment of moderate to severe TBI

• focus on ABCs

• investigate for serious neurologic injury: consult neurosurg

• consult for PM & R for rehab meds

• surgical intervention is indicated:

  • hematoma 10 mm + CGS of 2+ decline, pupils are fixed + dilated

• abx for infection, vaccination against pneumococcus

• scalp laceration: simple skull fracture with CSF

  • Leakage: elevate head, fluid restriction, admin of acetazolamine

patho/etiology of Basilar Skull Fracture

• occur at base of the skull

• MC occur through temporal bone + have increased risk of CSF risk

• occur in high-velocity injuries

• possible concomitant injuries; carotid dissection, damage to CN III, IV, VI

signs + sx of basilar skull fracture

• bruising overlying mastoid process (Battle)

• periorbital ecchymosis (racoon eye)

• CSF leak from subarachnoid space to paranasal sinuses resulting in clear rhinorrhea

• blood can build up behind TM

• CN palsies (1, 2, 3, 4, 5, 7, 8)

diagnostics + treatment for basilar skull fracture

• head + neck should be immobilized until imaging can be performed

• CT to find fracture

• consult neurosurg

patho/epidemiology of epidural hematoma (intracranial hemorrhage)

• found between dura + skull

• associated mainly with skull fracture that lacerates a MCA

• usually in pediatric + younger adult population

signs + sx of epidural hematoma

• “lucid” interval (loss of consciousness for a bit)

• deterioration as bleeding continues

• HA, N/V, confusion, seizures, aphasia

• “down & out” eye with blown pupil from CN III palsy

• Cushing reflex: HTN, bradycardia, respiratory distress

diagnostics + treatment for epidural hematoma

• CT: convex shape/focal wedge on the side

• shows hyperdense for acute bleed

treatment

• small: resolves spontaneously

• large: urgent surgical intervention w/ neurosurg

patho/etiology for subdural hematoma

• collection of venous blood between dura mater + arachnoid

• hematoma from tear in bridging veins from cortex to superior sagittal sinus or from cerebral laceration

• more in elderly + alcoholics with brain atrophy

• common mech is sudden accel-decel

• sx is longer

signs + symptoms for subdural hematoma

• presents with 14 days of injury

• most symptoms within 24 hours

• HA, dizzy, weak, nausea, vomiting

• focal neurologic deficit (hemiparesis/hemisensory disturbance)

• gradual decline in mental status

3 types of subdural hematoma

1. Acute: presents 1-2 days after onset, with hyperdense blood on CT

2. subacute: presents 3-14 days after onset

3. chronic: presents 15 days or longer after onset, with insidious HA, cognitive impairment, neurologic deficits, and seizures

diagnosis and treatment for subdural hematoma

• CT scan: crescent shaped hematoma

Tx

• surgical intervention if neurologic decline

• surgery to release pressure by drilling hole (burr hole) or doing a craniotomy/ectomy

• >10 mm thick or midline shift shift >5 mm

• pupil dilated + fixed

• decline of GCS >2

patho/etiology and signs/symptoms of subarachnoid hemorrhage

• between pia and arachnoid

• MCC: ruptured intracranial aneurysm

• raised suspicion for AVM/aneurysm

signs/sx:

• severe HA (“worst HA in life”, “thunderclap” HA)

• N/Vomiting

• decrease level of consciousness, neck stiff, focal neurological deficit

diagnosis for subarachnoid hemorrhage

• after 72 hours, rate of CT scan increases

• Head CT

• if CT is normal, do LP

  • xanthochromia (RBC in CSF fluid)

• confirm SAH have cerebral angiography to identify potential underlying aneurysm

Tx for subarachnoid hemorrhage

• 1st priority: secure aneurysm ASAP

  • endovascular coiling to block blood flow to aneurysm

• neurosurg clipping to close aneurysm

  • follow with serum electrolytes + osmolality

  • supplemental oral salt + IV

• anticonvulsants: seizure prevention

• vasospasm prevention (Nimodipine)

• control BP

red flags of headaches that indicate serious etiology

• sudden-onset headache

• first severe headache

• “worst headache ever”

• vomiting from HA

• neck pain/stiffness

• papilledema

• known systemic illness

• >55 years

• focal neuro deficits

types of primary headaches

• migraines (w/ or without aura)

• tension

• cluster

patho/etiology if different migraines

• before age 30

• family hx

• 3x in female

• unilateral

without aura (common migraine)

• 85% of migraines

• HA 4-72 hrs

• unilateral

• mod to severe pain intensity

• nausea and vomiting

• photo + phonophobia

with aura (classic migraine)

1. 15%

2. aura lasts < 60 min

3. vision change (scotomas, photopsias)

4. unilateral weak

5. slurred speech

6. tremor, vertigo

7. transient aphasia ( impacts speech)

migraine variants (2 types)

• has aura without HA

Basilar artery migraine

• blindness or visual disturbances through both visual fields

• dysarthria, disequilibrium, tinnitus, perioral parathesias

• followed by unilateral HA, Nausea, and vomiting

  Ophthalmoplegic migraine

• HA, eye pain, CN III palsy (no abduct)

diagnosis of migraine HA

• MRI to rule out secondary causes

• routine labs to r/o other disorders like infection, stroke, seizure, or toxins

• excess dopamine

• recognize triggers (when they occur)

tx for migraine

• acupuncture, maintain regular sleep, moderate exercise

• 1st line: NSAIDS (take at time of migraine)

• 2nd line: triptans → cause vasoconstriction

  • act rapidly (1 hr) + effective

  • combine with NSAID

  • don’t us if pt has vascular disease, brainstem migraine, hemiplegic, or pregnant

• older tx is ergotamine

  • may cause rebound HA + not for pregnancy

• antiemetic, IV ketorolac

prophylaxis tx for migraine

• frequent severe migraines (>4 episodes pr month or lasting longer than 12 hours)

• 1st line

  • beta-blockers (propanolol) → most effective

  • TCAs (amitriptyline): makes you tired

  • anticonvulsants (valproic acid, topiramate) seizure

• 2nd line

  • Ca++ channel blockers (verapamil) if beta-blockers not effective

• proper sleep, avoid food triggers

• Botox for chronic migraines

patho/etiology, s/sx, tx for menstrual migraine

• occurs between 2 days before or last day

• cause: estrogen withdrawal

tx:

• low-dose estrogen therapy during menstruation

• NSAIDS

• Triptans

• oral magnesium

patho + etiology for tension HA

most common type of HA

• bilateral, no pulsatile, and without systemic sx

• common in all age groups

risk factors: insomnia, stress, anxiety

• persists hours to days slowly

signs/sx and diagnostics for tension HA

• bilateral, nonpulsatic, and without systemic sx

• pain as bilateral tight, bandlike discomfort

  • “band around my head”

  • no nausea/vomiting and photophobia

• builds slowly: persists hours or days

Diagnostics

• tenderness of temporalis, masseter, post cervical, trapezius, sternocleidomastoid, and occipital muscles

• imaging does not show much, but done if suspicious

treatment for tension HA

• due to stress; local heat + muscle relaxants

• simple analgesics like NSAIDs, ASA, tylenol

• ketorolac IM used in out pt or hospital setting if sx are severe

• amitriptyline for chronic tension: type HA prophylaxis

patho/etiology of cluster HA

• Rare form of primary HA; 0.1%

  • in middle aged men

• RF: alcohol, smoking, stress, nitroglycerin, chocolate

• cluster of sx: Horner’s syndrome, ptosis, tearing

signs/sx and diagnostics for cluster HA

• occurs unilateral

• tearing, sweating, conjunctival hyperemic, miosis (eyelid droops)

• “suicide HA”

• retroorbital searing pain

• lasts 15-180 minutes

• may occur several times a day

• pace incessantly as not relieved by rest

diagnostics

• r/o other causes of acute head + facial pain

• brain MRI for initial diagnostics

treatment for cluster HA

• abortive tx: 100% O2 for this HA @ 12 L pr min with non-rebreathing mask

• 2nd

  • subcutaneous injection of sumatriptan

• prophylactic

  • verapamil

  • lithium (anti-seizure)

  • prednisone

  • deep brain stimulation of post hypothalamic gray matter

patho, sx, tx for chronic paroxysmal hemicrania

• unilateral, severe, short-lasting HA that is often retroorbital + association with lacrimation + nasal congestion

• line cluster HA sx: shorter, more in females

tx

• oral NSAIDS (indomethacin)

cluster HA vs Chronic paroxysmal hemicrania

Cluster

• males

• lasts longer and less frequent

CPH

• rarer

• more in females

• shorter + more frequent

patho, signs/sx, dx, tx for primary cough HA

• Severe head pain may be caused by cough

• lasts for several minutes

• benign; indicate post. fossa mass lesion

diagnostics

• brain MRI or CT to see any tumors

• self-limiting: persist for many years

tx

• indomethacin 75-150 mg to provide relief (NSAIDs)

patho, signs/sx, diagnostics, tx for lumbar puncture HA

• onset 48 hrs after LP (can be delayed up to 12 days)

• cause: leakage of CSF through puncture hole in membrane surrounding spinal cord

  • leakage decrease pressure by spinal fluid on brain + spinal cord → HA

• relief by lying flat

tx

• IV or oral caffeine (500 mg IV)

• epidural blood patch

signs/sx, patho, dx, tx, for medication overuse/rebound HA

• ½ patient with daily chronic HA

• chronic pain/severe HA becomes more unresponsive to medication

• RF: ergotamine, triptans, meds with butalbital, and opioids responsible when taking 10x a week

  • ASA, NSAIDs, tylenol, if more than 15 days

• help with analgesics withdrawal

temporal arteritis (GCA) and correlation to HA

Signs/sx

• HA

• jaw claudication

• scalp tenderness

• head/neck pain

• visual sx (amaurosis fugac)

• onset @ 79

labs

• elevated ESR, CRP, Temporal biopsy

tx

• steroids (prednisone) to decrease flare-ups

• tocilizumab to reduce prolonged use

stages of altered consciousness

• Lethargy: arousal is decreased, but pt maintains ability to be aroused spontaneously with vocal or light touch stimulation

• obtundation: reduction in arousal; minimal responsiveness to touch or voice

• stupor: severe arousal with minimal responsiveness to vigorous stimuli

• coma: unarousable and unresponsive

• brain death: no brain function

patho, S/Sx, tx for delirium

• acute state of confusion and decreased arousal alternating with periods of agitation

• RF: pre-existing cognitive impairment

• MC with elderly

s/sx

• fluctuating levels: arousal-drowsy-agitated (ADA)

Dx

• based on clinical presentation

tx

• tx underlying cause

patho, S/sx, tx for encephalopathy

• acute side of confusion + impaired attentiveness caused by metabolic derangement

• causes: metabolic or drug-related (ammonia)

• caused by hepatic encephalopathy

sx

• develop more slowly + can be acute or chronic

tx

• reversible or permanent impairment

• dependent on cause

describe coma

• depressed level of consciousness to extent that pt is completely unresponsiveness

• specific to pt

  • unable to be awakened

  • fails to respond to pain, light, or sound

  • no sleep-wake cycle

  • does not take voluntary actions

    • typically < 2-4 weeks/ can be up to 12 months

    • coma may be transient or permanent

• pt is alive with brainstem function and reflexes

describe persistent vegetative state (PVS)

• person loses higher brain functions and unaware of their surroundings, but retains non-cog function and regular sleep wake cycles

• periods of waking + exhibit some reflexive movement

distinguish PVS from Coma

PVS

• eyes opened

• not meaningful interacting

• eyes do not track external stimuli

• can become coma to death

Coma

• no eyes opened

• no movement

Describe Locked in Syndrome

• pseudocoma

• condition in which pt is aware but unable to move or communicate verbally

• vertical eye movement; up + down + blink

• intact conscious

• lesion to brainstem, often from occlusion of basilar artery with acute ischemia to pons

• damage to corticospinal + bulbar tracts

• mouth + tongue paralysis

• poor prognosis

describe minimally conscious state (MCS)

• severely altered consciousness but evidence of self-awareness or awareness of environment

• presence of minimal but definite behavioral evidence of consciousness

• functional recovery: basic verbal, contex appropriate gestures, emotional responses

• temp or permanent

• persists after 12 months, severely disabled

describe catatonia

• unresponsiveness due to psych disorder with disturbance of motor behavior but maintained consciousness

• stuporous + hyperexcitable forms exist

• stuporous form MAY resemble coma

• behavioral disturbances

  • mutism, posturing, waxy flex, catalepsy (in a trance)

Glasgow Coma Scale scoring

• 13-15 pts

  • mild

  • normal to lethargic; mildly disoriented

• 9-12 pts

  • moderate

  • lethargic to obtunded, follows commands with arousal, confused

• 3-8 pts

  • severe

  • comatose, no eye opening or verbalization, does not follow commands, decorticate or decerebrate posturing

description of ocular findings

• unilateral dilated pupil

  • CN III compression

• bilateral dilated pupils

  • midbrain injury

• irregular pupils

  • orbital trauma

• conjugate gaze deviation

  • frontal lobe lesions

• small/pinpoint

  • point injury, opiate administration

ocular findings in altered mental status/coma

• pupils: doll’s eyes

• horner syndrome: hypothalamic disease

• small but reactive: bilateral diencephalic involvement

• ipsilateral pupillary dilation with no direct or consensual response to light: compression of CN III

• smaller than normal but responsive to light: metabolic encephalopathies

• fixed + metabolic: overdose with atropine or scopolamine

• pinpoint + responsive: opioid overdose

• PAM

  • ptosis, anhidrosis (no sweat), miosis

assessing respiratory patterns

• cheyne-stokes: episodes of deep breathing alternat with periods of apnea

• hyperventilation: brainstem tegmentum

• apneustic breathing: prominent end resp pauses

• damage @ pontine level: basilar artery occlusion

• lower pontine legmentum + medulla

patho/etiology of bacterial meningitis

• sudden inflammation of meninges, the three membranes surrounding brain and spinal cord

  • dura mater, arachnoid mater, and pia mater

• fatal if untreated

• relatively rare in US

• outbreaks in close quarters

• diffuses through BBB

• vascular injury → disruption of BBB

• disruption of normal CSF flow

• gain access to CSF through blood

pathogens of bacterial meningitis

• neonate

  • group B strept, E. coli, listeria

• children > 3 months

  • N. meningitidis, s. pneumoniae, H. influenzae

• adults (18-50)

  • s. pneumoniae, n. meningitis, h. influenzae

• elderly

  • s. pneumoniae, n. meningitis, l. monocytogene, gram (-) bacilli

• immunocompromised

  • l. monocytogens, gram (-) bacilli, s, pneumoniae