neurology domain guide

8/13/2019 Neurology Domain Guide

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Diseases of Peripheral n (neuropathies)

Age of Onset Location of Lesion Pathogenesis Clinical Presentation Gross/Micro

Pathology

Diabetic PeripheralNeuropathy

Adult-onset Symmetric distal

polyneuropathy

Segmental demyelination Decreased sensation in distal extremities Axonal neuropathy

Segmental demyelination,

thickening of endoneurialarterioles, hyalinization

Werdnig-Hoffman

Disease

(SMA type I)

At birth orw/in 1st 4

months

Degeneration of LMN Autosomal recessiveMutation in SMN1

(missing exon 7)

LMN lesion; gen weakness, hypotonia, mwasting, tongue fasciculations; “floppy

baby

Atrophy of ventral horns/nroots; neurogenic atrophy

Amyotrophic

Lateral Sclerosis

Middle

aged/elderly

UMN & LMN Autosomal dominant

Degeneration of LMN andUMN

UMN lesion deficits (hyperreflexia,

Babinski) LMN lesion (fasciculations,wasting, weakness)

Atrophy of ventral horns/n

roots; Wallerian degen

Guillain-Barre

Syndrome

Degeneration of

peripheral nn

Immune-mediated

disorder

Ascending paralysis; weakness in distal

limbs w/ rapid advance to proximal mm,

slow n conduction

Chronic inflammation, seg

demyelination

Charot-Marie-Tooth(HSMN type 1) Childhood,earlyadulthood

Degeneration ofperipheral nn Autosomal dominantChromosome 7duplication; PMP 22

Distal m weakness; inverted champagne-like calf; pescavas, hammertoes Onion bulb-Segmentaldemyelination-remyelination;

Neurogenic atrophy: atrophy in m fibers due to pathological changes in n or PNS

Denervation atrophy: myocytes atrophy due to axon/myelin sheath degeneration

Wallerian degeneration: axonal degeneration distal to point of axonal damage or cell body damage

Disease of NMJ

Myasthenia Gravis NMJ Immune-mediated loss ofAch receptors

Begins with extraocular m weakness; ptosis, double vision; generalized weakness

Electrophysiological tests:nerve conduction and

electromyography; n/m

biopsy

Myopathies: have elevated creatine kinase and proximal weakness; random necrosis and/or m fiber regeneration

Neuropathies: distal weakness; group atrophy; fiber type grouping



Increased Intracranial Pressure and Herniation

Etiology Compression Clinical Features

Increased ICP Depends on age of pt and speed of expansionFactors depend on speed of expansion, age of patient;

>200mm water in LP

Headache, vomiting, pailledema maybe (swollen optic n), abducens n. palsyBlurred optic discs; focal neurologic signs: limb weakness

Cingulate gyrusHerniation

Herniates under the falxcerebri

Uncal Herniation Hemorrhage,

neoplasms,infections

Uncus herniates across tentorium

cerebelli -compress structures inpost fossa;

Compress PCA, midbrain cerebral

peduncle, CN III, brainstem downward

Ptosis, dilated pupil, fully abducted eye, fixed pupil, infarct of unilateral occ

lobehomonymous hemianopsia/hemianopia; Duret hemorrhages due to downwardbrainstem compression

Brainstem compression: central herniation or rostrocaudal deterioration

Cerebellar TonsilHerniation

Cerebellar tonsil herniation thru foramen magnum Compresses medullary respiratory centers leading to death

Midline shift Lateral displacement of diencephalon may produce decreased level of consciousness

Central Herniation

Rostrocaudaldeterioration

Supratentorial

space occupyingmass; downward

displacement of

brainstem

Small reactive pupils (loss of sympathetic), Dilated, fixed (loss CNIII parasympathetics because the parasympathetics travel in the

PERIPHERY of CNIII), Midposition, fixed: compression of both III and midbrain (loss of sympa/para)Duret hemorrhages may also occur

Changes in consciousness (drowsiness, stupor, coma), resp changes; postural changes: Decorticate rigidity (leg extension/arm

flexion);

Decerebrate rigidity (leg/arm extension)

*Cheyne-stokes in diencephalon*Central neurogenic hyperventilation in midbrain

*Apneustic Respiratory in pons

*Ataxic Respiratory in medulla

* In infants, skull may expand and in elderly, brain may have atrophied due to old age, so may have more room for expansion.

Infections involving Nervous System

Etiologic Agents Pathogenesis Clinical Features Spinal

FluidChanges

Notes

Epidural/Subdural Abscess or

Empyema

Pyogenic bacteria:

step, staph

Direct inoculation or spread from nearby infection Localized collection of

pus

Complications:

HydrocephalusEdema

CN palsies

Thrombosis

Brain abscess

Seizures

Meningitis Bacterial

Pyogenous

Homogenous spread

from body to brain;direct inoculation,

direct spread

Purulent exudate in SAS w/

PMN, bacteria, vasculitis; Edema,cellular infiltration of CN/sp

roots

Hydrocephalus, edema

ICP, seizures,thrombosis, abscess,

CN palsies

P

glucose

protein

cells

ViralAcute Lymphocytic

Aseptic Normal PNormal glc



protein

cells

Fungal

Chronic

Candidiasis,

Cryptococcus,

tubercle bacillus,

T. pallidum(syphilis)

Exudate, mononuclear infiltrate,

vasculitis

Granulomatous

P

glc

ptn

cells

Viral Encephalitis Depend on age,

location of pt,

time of year

Meningoencephalitis,

encephalomyelitis

Homogenous spread

after viremia, spread

along nn

Arthropod-bourne VE

Epidemic; 10% by arbovirus

Perivascular cuffing,

neuronal/hemorrhagic

necrosis, microglial

nodules/proliferation,

inclusion bodes

HSV Type 1Tx w/ acyclovir, effect mood,

memory, behavior

RBC’s

present

HSV Type 2

Meningitis or encephalitis

Rabies

Negri bodies: inclusions in

pyramidal neurons ofhippocampus

VZV shinglesgranulomatous

arteritisinfarcts

CMV common in opportunisticviral pathogens in HIV pts

Poliomyelitis infect antieriorhorn neurons, motor deficits,

flaccid paralysis

Intracranial Abscess Pyogenic bacteria

(Staph/strep)

Intracerebral inflammation called granulomas

Homogenous spread; caused by acute bacterialendocarditis, cyanotic congenital heart disease; Discrete

lesions w/ liquefactive necrosis, with zone of fibroustissue

Progressive focal

deficits, gen signs ofincreased ICP

pressure,few cells,

WBC/ptn;

normal glc

HIV-associated

CNSSyphilis

Meningovasculitis Infiltration of meninges & vessels by lymphocytes/

plasma cells

Meningitis, or vascular

occlusion; similar to

low-grade meningitis

or stroke

General Paresis Atrophy, loss of cortical neurons in frontal lobes, gliosis,

prolif microglial cells, perivasc lymphocytes, spirochetes

Mental changes,

progressing todementia, headache



Tabes Dorsalis Inflammation of meninges in SAS/dorsal n roots;

wallerian degeneration

Lightening pains,

sensory deficits, loss

PT/MVP; argull-robertson pupils

Progressive Multifocal

Leukoencephalopathy

In pts w/

associatedimmune

supp/chronic dis

Viral encephalitis

Latent infection of polyomavirus in kidney/Blymphocytes

Demyelination; inclusion oligodendroglia nuclei

Intellectual

deterioration anddementia, visual, motor

dx, abnmvmts

Normal Death in 2-6

mos

SubacuteSclerosingPanencepha

litis (SSPE)

Progressiveencephalitis

associated with

altered measlesvirus

Persistent but nonproductive infection of the CNS byaltered measles virus; inclusion bodies in

oligodendroglia, neurons, astrocytes, perivascular

cuffing, neuronal loss, gliosis, demyelination

Intellectualdeterioration, seizures,

spasticity of limbs,

progressive personalitychanges

↑gammaglobulin

↑Ab titer

againstmealses

Death inseveral years

CNS development dx, including malformations, perinatal brain injury, cerebral palsy

Pathology Causes Clinical Features Types Diagnosis

Cerebral Palsy Intraparenchymal

hemorrhage originating

in germinal matrix

Asphyxia, maternal high

bp. Diabetes, trauma,

infarctions, hemorrhages

Ataxia/athetosis,

dystonia, paresis,

spasticity

Spastic: increased m tone;

stiff/jerky mvmts

Correctly diagnosed bet 12-24

mos

- floppy/limp body OR stiffness of

arms/legs in 1st few mos-no smile by 3 mos

-poor head control at 3-4 mos

-no sit up by 8 mos

-difficulty standing at 12 mos

-inability to walk by 18-20 mos

Ataxic: decreased m tone/

poor coordination

Athetoid: due to

hyperbilirubinemia; can’thold selves upright

Germinal Matrix

Hemorrhage(Intraparenchymal)

Subependymal matrix hemorrhages; due to cerebral hypoxia between 25 th and 35th week of gestation

Periventricular

Leukomalacia

Infarcts occur in the periventricular white matter; cyst may form

Chalky yellow plaques of discrete regions of white matter necrosis and calcificationUlegyria Due to ischemic lesionssulci bear the burnt of injury thinned-out, glioticgyri

Cerebrovascular Diseases Epidural Hematoma Subdural Hematoma

Disease Location/Etiology Pathogenesis Notes

Stroke Ischemic

Thrombosis

Embolism

1% of head trauma admin;

4:1 male to female; rare b4age 2 & after age 60

Bilateral in 10% of cases;

more common in elderly

HemorrhagicSAH, ICH

Acute:Trauma,

contusion

Chronic:Infants,

elderly, devHypoxic Pyramidal cells of hippo, Decreased bld flow, anoxic poisons Man in barrel Death may occur 2-12



Encephalopathy

(border zone: watershed

infarcts)

pukinjie cells of

cerebellum, GP neu

(CO, CN, CS2, hypoglycemia) syndrome hours after injury; causes

uncal herniation or dnwd

over mos,

dementia

Focal CerebralIschemia

Thrombotic

Due to focal cerebral

arterial occlusion

Atherosclerotic plaque

formation, coagulability

of blood, vasc occl,ateriopathy, cerebral

amyloid angiopathy, drugabuse, aneurysm

Gross Path: 6-12hrs: no lesion discerned. 48 hrs: tissue

pale, soft, swollen, gray-white matter jxn indistinct. 2-10

days: gelatinous, friable. 10d-3wks: tissue liquefiesMicro Path: 12hrs: neu nuclear pyknosis, cytoplasmic

eosinophilia; 1-3days: PMN, cap prom, endo swell,

vacuolation of white matter. 3-5days: m appear. 7-21d:astrocytes proliferate, gemistocytic

Pale Infarct

Non-hemorrhagic

Shrinkage, distortion of structures, cysts, compensatory

ventricular enlargement

Ischemic neu (eosinophilic/red neurons); capillaryprominence, vacuolation of white matter, macrophages,

astrocytes become gemistocytic

Ischemia due to

Embolism

Thrombotic embolus in

MCA

Sudden onset of focal

impairment

Hemorrhagic infarction;

characterized by petechial

hemorrhages

Skull fracture rupture of

MMA-rapid bleeding mass

effect

Shearing of bridging veins;

accum around parenchymal

laceration; 2∘ to acc-

deceleration injury

Venous or Dural Sinus

Thrombosis

Blood stasis in large vv/venous sinuses leads to infarction; increased pressure

disrupts capillaries causing blood to enter infracted areas

Unconsciousness, lucid

interval, coma, focal signs,

ICP, death may occur 2-12

hrs due to herniation;obtundation, contra

hemiparesis, ipsi pupillary

dilation

No lucid interval

Nonlocalizing, headache,confusion, progressive

neurologic deteriation

Chronic: seizures,

headache, confusion,behave changes, signs of

ICP

Spontaneous

INtraparaencymalHemorrhage

Hypertension; others are

AV malformation,

ruptured aneurysm,

amyloid angiopathy,

leukemia--basal ganglia/thalamus

and pons and cerebellum

Arteriolosclerosis ; thickening of

vessels, hyalinization, form of sm

aneurysms; Charcot-Bouchard

Aneurysms

Uncal herniation-brainstem

compression & 2 Duret brainstemhemorrhages

AneurysmsBerry/Saccular/

Congenital

Occur at bifurcations ofvessels at base of brain

Rapidly developing severe headache Common cause ofSAH

Biconvex high density;sharply defined; rarely

cross sutures, may cross

midline & tentorium

Crescentic mass of highattenuation, may cross

sutures; do NOT cross

midline; less dense thanEDH, but high density on CT

Vascular

Malform.

AVM Tangles of abnormal vessels

Seizure, headache, focal neurological signs

Remove blood & associated

organization tissue

AV Shunt Causes high output cardiac failure; generally involves vein of Galen and MCA or PCA

Lacunes Infarcts Small infarcts, associated with HTN ; tissue loss with scattered lipid-laden

macrophages and surrounding gliosis



Slit Hemorrhages Rupture of penetrating arterioles small ICH resorption leaving slit-like cavity

Hypertensive

Encephalopathy

Rapidly evolving syndrome of severe HTN

Headache, nausea, & vomiting

Seizures

Epidemiology/

Demographics

3% of all ppl living to age 80 will be diagnosed w/ epilepsy; highest incidence in young children and elderly ; 70% well cont rolled w/ meds,

30% w/ intractable epilepsy

Etiology Newborn Asphyxia, intracranial hemorrhage, hypocalcemia, hypoglycemia, hyperbilirubinemia, water intoxication,inborn errors of metabolism, trauma

Infancy Febrile (5 mos-5 yrs), CNS infection, trauma, congenital defects, inborn errors of metabolism

Childhood Trauma, CNS infection, arteriovenous malformation, congenital defects, tumor

AdolescenceEarly Adulthood

Trauma, CNS infection, tumor, arteriovenous malformation, drgus/alcohol

Late Adulthood Drugs/alcohol, trauma, tumor, vascular disease, degenerative disease, CNS infection

Generalized Seizures Partial Seizures

GeneralFeatures

No aura, postictal confusion (not in absence/myoclonicseizure); may have bowel or bladder incontinence, tonguetrauma

Simple: no alteration in level of consciousness, no postictal stateComplex: alteration (not loss) in LOC; may have aura, postictal confusion

Clinical

manifestations/

course

Tonic m. rigidity (extension or flexion) Motor Tonic or clonic, versive head or eye movements

Clonic Gen. m. jerking activity Sensory Positive phenomena: parasthesias/dysesthesias, visual

halllucinations

Tonic-Clonic

Grand mal

Rigidity followed by jerking; ictal scream;

apnea may appear

Autonomic/

Visceral

Gustatory, olfactory, epigastric fullness, nausea, pupillary

changes

Atonic

Petit mal

Bried loss of m. tonefall or head drop Psychic Déjà vu, jamais vu, depersonalization

Absence Staring spell 5-15 sec; provoked by

hyperventiliation (only in childhood);no postictal

Myoclonic Localized/widespread jerking mvmts;

infantile, juvenile

Diagnosis CT or MRI, EEG, hematology (CBC, electrolytes, Ca, Phosphate)



Intracranial Neoplasms

PrimaryTumors

More in adultsthan in children

Usuallysupratentorial;

can spread viaCSF, but no

spread beyondCNS

ChildrenICP may

be onlysign

presented

Pilocytic astrocytoma Cystic lesion with mural nodule of tumor; good prognosis; grade 1; incerebellum

Medulloblastoma

Most common

Grade 4; usually in cerebellum; poorly differentiated neoplasm;

truncal ataxia, ICP; seeding thruout SAS; mitotically active prognosis:

gloomy

Ependymoma Mostly in 4th ventricle; due to ICP; solid tumor, true ependymal

rosettes

Retinoblastoma Sometimes bilateral, may extend to optic n; good prognosis

Neuroblastoma PNS, often in adrenal gland; poor prognosis

Adult

50-75%

areprimary

Gliomas Astrocytomas

Grade 2: diffuse

Grade 3: anaplastic

Grade 4: glioblastoma

Cerebral hemispheres; low grades=firm, white/gray, poorly

circumscribed, infiltrates & distorts brn tissue; grade 3-4: well

circumscribed, infiltrates widely, many colors due to hemorrhage,necrosis, &cysts

Oligodendrogliomas Often in cerebral hemispheres; “fried egg” appearance; slow-growingtumor

Ependymomas Within skull are rare; often in lateral ventricles more common in the

spinal cord

Primary Brain Lymphoma From B lymphocytes in CNS to deep cerebral hemispheresheadache,

seizures; soft, multiple separate nodules

Germ Cell Tumors Origin: ectopic germ cells; location: midline (pineal/suprasellarregion); good prognosis

Pineal Parenchymal Tumors Clinical effects: visual disturbances and headache

Meningiomas Well-circumscribed mass, no invasion; whorls or sheets of

meningothelial cells, psammoma bodies

MetastaticTumors

Frequentlymultiple,

distributed by

volume,

supratentorial

Spread via CSF

Intra-Axial

Tumors

Meningioma

Metastasis

Schwannoma

Neurofibroma

Extra-Axial Astrocytoma Grade 2: nuclear pleomorphism (solid, infiltrating, may show Survival over 5 years is rare



Tumors cystic change

Grade 3: plus mitotic activity

Grade 4: Glioblastoma: Necrosis with palisading, and/or vascularendothelial proliferation; may show hemorrhage

Ependymoma Usually in spinal cord in adults (4th ventricle in children) Prognosis related to resectibility

Oligodendroglioma

Can be associated with loss of chromosome 1p and 19q

Metastasis

Diagnosis Always cranial MRI with gadolinium enhancement

Von-

HippelLind

auSyndrome

Mutation in tumor

Multiple CNS hemangioblastomas

Increased renal cell carcinoma

Hemangio

blastoma

Thin-walled vessels w/ vacuolated cells; cystic lesion with mural nodule usually in cerebellum; 10% of patients have polycythemia when tumor cells make

erythropoietin

Neurofibro

matosis I

Mutation in Chromosome 17; peripheral neurfibromas may show malignant degeneration; pilocyticastrocytomas (optic nerve)

Neurofibro

matosis II

Multiple meningiomas& bilateral acoustic schwannomas, ependymoma, mutation on chromosome 22-merlin protein

TuberousSclerosis

Cortical tubers, angiomyolipoma of kidney, renal cell carcinoma, renal/hepatic cysts



Movement Disorders

Disease Clinical Features Pathology Epidemiology Differential Diagnosis

Hypokinetic Movement Disorders

Parkinson

Disease

Rigidity, gait instability, resting

tremor, bradykensia

--mood dx, later dementia,dysautonomia

--olfactory dysfxn, constipation,

autonomic, dysfxn, sleep dx,

dep/anxiety

Degeneration of

pigmented brainstem

neurons insubstantianiagra, lewy

bodies, ↓Da in striatum

11/100,000 in general

population

50/100,000 over age 50Cumulative lifetime risk:

2.7%; Slightly morecommon in men

Risk Factors: age, severe

head trauma, familyhistory, env exposure, low

uric acid

Protective factors:

estrogen, caffeine, heavyalcohol, smoking, NSAIDS

Secondary

Parkinsonism

Drug-induced, post-traumatic,

post-infectious, immune-mediated,

vascular, normal pressurehydrocephalus

Other Tremor

Syndromes

Essential, myoclonic, dystonic

Akinetic-Rigid

Syndromes

Progressive Supranuclear Palsy-

Accumulation of hyper-

phosphorylated tau ptn in neuron-CBT/CST signs, wide unblinking

face, axial rigidity, dn gaze paresis

Multiple System Atrophy

Cerebellar signs, dysautonomia,CST signs, stridor

Corticobasal DegenerationProgressive asymmetric rigidity,

apraxia, alien limb, rarely gaze

palsy

Diffuse Lewy Body Disease

Hereditarydisorders w/

Parkinsonism

Wilson’s: AR, deficient copperexcretion, ↑serum/urine copper

hepatic failure, basal ganglia-

akinetic-rigid, wing-beating tremor

Huntington’s

Hyperkinetic Movement Disorders

Tremor Repetitive rhythmic alternating contractions of agonistic/antagonistic muscles: terminal, resting, postural/action, wing-beating tremor

Dystonia Sustained and/or phasic contraction of m causing abnormal posture or repetitive movements

Myoclonus Rapid, lightning-like m contraction producing irregular jerking

Chorea Brief, irregular jerking movements flowing from on body part to the next (metabolic, auto-immune, degenerative, vascular, drugs)Huntington’s Disease: expansion of CAG: chorea, dementia, psychiatric, cerebellar features, prominent atrophy of caudate nuclei

Hemiballismus Rapid, large amplitude, unilateral, proximal flinging movements

Tics Repetitive, stereotypic, brief semi-involuntary movements



Demyelinating Diseases

Disease Age of Onset/ Epi Etiology & Pathogenesis Pathological Changes Diagnosis Treatment

Multiple Sclerosis

Autoimmune Dx

Age of onset: 20-

50; more common

in women and

Caucasians30-300/100,000

CD4 TH1, TH17 cells react

against self-myelin Ag &

secrete cytokines, B cells, T

cells, & innate immunesystemdemyelination

Initially: Optic neuritis

Plaques of demyelination in

white matter of brain/sp cd, not

PNS; # of oligodendrocytes,gliosis, activation of microgliaand macrophages

Remitting and relapsing

MRI, CSF analysis : oligoclonal

bands, IgG

CSF: gamma globulin elevated,

oligoclonal gamma globulinbands

Ag non-selective

immunomodulators

: copaxone, inhibits

myelin basicprotein (MBP)

Neuromyelitis

Optica (Devic Dis)

Development of both optic neuritis and spinal cord demyelination at similar points in time

Acute Disseminated

Encephalomyelitis

Rapidly progressive diffuse demyelinating disease, develops 1-2 wks after viral infection

Demyelination in perivenous distribution

Acute Necrotizing

Hemorrhagic

Encephalomyelitis

Common in young adults and children, usually in upper resp infection; CNS demyelination

Central Pontine

Myelinolysis

Demyelination in basis pontis and pontine tegmentum; classically associated with rapid correction of hyponatremia

Visual System Disorders

Three Vital Signs Visual acuity, Pupils, Pressure

Glaucoma

Optic Neuritis

Giant Cell Arteritis Headache, jaw claudication, weight loss, malaise…

A true neuro-ophthalmic emergency

Traumatic Optic neuropathy

Vestibular System Disorders

Disease ClinicalFeatures

Central Causes Peripheral Causes

Vertigo

Sensation of movement of self/env, often

rotary. Mismatch of visual, vestibular, &

sensory proprioception

Nystagmus,

(hallmark)

Vertigo, diplopia, weakness, and/or

numbness

Vertigo, hearing loss, tinnitus

TIA not only vertigo, but combo of

diplopia, dysarthria, numbness,

incoordination

Benign Paroxysmal Positional Vertigo

Vestibular most common cause of vertigo; Dix-Hallpike

testing (pt rapidly moved from seated position to lying position

Tumor or mass rarely with isolatedvertigo; tx w/ traditional prophylactic

migraine meds

Vestibular Neuritis monophasic episode of vertigo; days toweeks, nausea/vomiting; tx w/vestibular suppressants

(meclizine, diazepam, Dramamine, lorazpam)

Migraine Meniere’s Disease endolymphatic regulatory dysfunction; last

hours; ear pressure/fullness, change in tinnitus & hearing



function

Multiple Sclerosis important cause Trauma

Nervous System Trauma

Etiology Clinical Manifestation Notes

Concussion Trauma Transient acute unconsciousness,headache, cognitive and sleep

disturbances, vertigo

Not an anatomic lesionNo evidence of permanent structural damage

Contussion Trauma – most common:orbital gyri, temp/occ pole

Areas of hemorrhagic necrosis,Brain moves linearly or rotates,

slam into skull

Coup lesions, counter coup, intermediary lesions

Diffuse Axonal Injury Trauma; present in 35%head trauma deaths

Located in deep white matterregions, Diffusion of tensor imaging

Major cause of prolonged traumatic coma, and poorneurological outcome

Spinal Cord Lesions(Direct v. Indirect)

Blow to back of neck ortrunk

Trauma to C4, C5, C6, C7,

T1 or T12, L1, L2

Sensory loss of sensation in aspecific dermatone indicated

location of lesion

Macrophages, gliosis, loss of architectureContusions, Wallerian degeneration

Headache

Epidemiology Duration of

Episode

Characteristics Location Treatment

Tension Both gendersAge 20-60

30 min-7 days Progresses throughout day, no aura, nophonophobia/photophobia, no N/A,

pulsating, tightening, pressing, no

aggravation by exertion

Bilateral Regular meals, hydration, rest, removestress, anxiolytics

Migraine FemaleAge 20-50

No aura: 4-72hrs

Aura: 2 or

more attacks

Can be with or w/o aura

Aura: N/V, photophobia, phonophobiaUnilateral Abortive

NSAIDS,

antihistamines,

α-adr blockers,

occ/supra-orbital n block

PreventiveAnti-depressants,

anti-convulsants, β-

adr blockers,

neuroleptics

Cluster Male Histamine mediated

Eye swollen and red, lacrimation, ptosis,

miosis, eyelid edema, nasal congestion,rhnorrhea, facial sweating

Unilateral Ergotamines,

lidocaine,

prednisone,

100% O2,

sumatriptan

Lithium, topiramate,

ergotamine

verapamil, sodiumvalporate

Paroxysmal hemicrania Female No frank Horner’s syndrome; extremelyresponsive to indomethacin

NSAIDS, salicylates

Doesn’t respond to O2



Secondary Headaches

Vascular Sentinel bleed (AVM, SAH), stroke, arteritis, carotid/vertebral dissection, venous/sinus thrombosis, arterial hypertension

Sentinel “Thunderclap” Headache: “worst headache of life”, ruptured aneurysm

Giant Cell (temporal)

Arteritis

Older patient Achiness in jaw, neck, palpate artery, get sed rate, CRP

Trauma-associated Subdural hemorrhage, SAH, concussive, post-concussiveIntracranial Disorders Increased ICP w/ mass, benign intracranial HTN, intracranial infection, low ICP even

Metabolic Hypoxia, hypercapnia, hypoglycemia, dialysis; non-cephalic infection, facial pain

Cranial Neuralgias Trigeminal Neuralgia“Tic Douloureux”

Severe pain in face, stabbing electric shock-like pain

2 to compression/inflammation of CN V

Tx: Carbamazepine, gabapentin, lamotrigine,baclofen; Surgery: rhizotomy, microsurgical

decompression, gamma knife

Glossopharyngeal Neuralgia Lancinating pain referred to tongue, ear

2 base of skull lesion, neck mass, vasc

compression

Anticonvulsants, microsurgical decompression

Occipital Neuralgia Aching pain, referred over scalp

2 to cervical trauma, arthritis, C1-C2

Unilateral Anticonvulsants, occipital n branch block,microsurgical decompression

Rebound Drug overuse, non-compliance, somatization, anger/anxiety, family dysfunction Discontinue offending analgesics, EDUCATE, hydrate,preventive pharmacotheraphy

Toxic, acquired metabolic, and nutritional dx of the CNS

Source or

Deficiency

Clinical Effects Notes

Lead

Motor peripheral neuropathy

Paints chips or paint

dust in homesCNS: in cerebral or cerebellar cortex

- Acute: seizures, ataxia, ICP

-Chronic: seizures, attention/mental deficits, loss of motor skills

PNS: in motor nn segmental demyelination; wrist-drop, slowed nconduction

Mercury Vapor Inhaled dental

analgams

Negligible

Methyl Fish Visual field constriction & ataxia

Ethyl Thimerosal in

vaccines

No evidence of damaging effects

Organophosphate Insecticide Insecticide Miosis, blurring vision, chest tightness, wheezing, GI, increasedsweating, increased salivation

Tx w/ Atropine

Organic solvents Workplace Organic affective syndrome: irritability, fatigability, difficulty in

concentrating, loss of interest

Mild chronic toxic encephalopathy: personality or mood change,

impairment in intellectual function



Severe chronic toxic encephalopathy: dementia with global

deterioration of memory & other cognitive functions

Botulinun Toxin Clostridia Mechanism of Action Clinical Effects

Cause deficiency of synaptic

transmission; must enter

axon terminal; preventsynaptic vesicles from

docking/fusing w/ presyn term

Nausea, dry mouth, double vision,

weakness, difficulty speaking and

swallowing; symmetrical flaccidparalysis

Tetanus C. tetani

Soils and spores

Tetanospasm; inactivates

synaptobrevin (block synaptictransmission that normally

inh MN

Lock jaw, opisthotonos

Carbon Monoxide Ventilation of

heating sources,

engine exhaust

Form carboxyhemoglobin

neuronal necrosis, and

apoptosis

Headache, myalgia, dizziness,

neuropsychological impairment

confusion, loss of consci, death

Methanol Toxicity Degeneration of retinal ganglion cells blindness

Ethanol Direct effects or 2

nutritional deficits

Effects are reversible; atrophy and loss of granule cells 1 in anterior

vermisUnsteady gait and nystagmus

Radiation Symptoms of intracranial mass, headaches, nausea, vomiting,

papilledema

Large areas of necrosis and adjacent edema

Wernicke’s encephalopathy & Korsakoff’s

syndrome

Thiamine, vitamin

B1 deficiency

Wernicke’s Encephalopathy: ataxia, confusion, ophthalmoplegia Located in

mammillary bodies ,periaqueductal gray

Korsakoff’s pyschosis: severe memory defects and confabulation

Pathological changes: vascular changes, capillary tortuosity,

prominence, endothelial swelling, petechial hemorrhage, neuronaldamage, macrophage response and gliosis

Alcoholic Polyneuropathy Numbness, paresthesias, weakness

Degeneration of both myelin & axons w/ axonal reaction in anterior

horn cells

Subacute combined degeneration Vitamin B12

deficiency

Peripheral neuropathy, optic neuropathy; associated with pernicious

anemia

Loss of MVP, LE weakness,DTR, babinski signs; degeneration of

post/lat columnsSpongy degeneration of white matter

Kernicterus Bilirubin toxicity Hypoalbuminemia is a causeAnoxia, acidosis

Hepatic encephalopathy Amidation of glutamateglutamine via glu synthetase takes place in



astrocytes

Brain edema, disturbances in consciousness & motor abnormalities

(pre-dominately involves glial Alzheimer type II cells in gray matter

Inherited Nervous System Metabolic Diseases

Location Deficit Result Genetic inheritance Clinical Expression

Neuronal Storage Diseases Gray matter Lysosomal enzyme(usually)

Accumulation ofenzyme substrate

Autosomal recessive Can range from focalabnormalities to mental

retardationLeukodystrophies Myelin and whitematter

Variety of clinicalexpression

Autosomal recessive

Mitochrondrial

Encephalomyopathies

Gray matter and

skeletal muscle

Oxidative

phosphorylation

Mitochondrial encephalopathy lactic acidosis

stroke-like episodes

Common Sphingolipidoses

Age of Onset Enzyme Deficiency Accumulated Product Clinical Signs Pathology

Tay-Sachs Disease

(type of Neuronal Storage Disease)

3-8 mos Hexosaminidase A GM2 gangliosides Psychomotor arrest,

exaggerated startle reflex,seizures, cherry red spot

Storage in central and

peripheral neurons

Metachromatic Leukodystrophy Earlychildhood Cerebroside sulfatase Sulfides Progressive mental and motordeterioration, peripheral

neuropathy signs

Myelin deficit in CNS/PNS,storage in glia

Krabbe Disease 3-6 mos Galacto-cerebrosde

β-galactosidase

Galacto-cerebroside Mental and motor

deterioration, seizures,irritability, crying

Myelin deficit; globoid cells

(large nucleated macrophages)

Degenerative Diseases

Age of

Onset

Location of

Lesions

Clinical Features Gross/Microscopic Pathology Diagnostic

Tests

Alzheimer’s

Disease

>60 years

Early: 40-60

Cortex,

hippocampus,entorhinal,

perirhinal cortex,basal forebrain

Memory loss, dementia

Gait normal, no focal weakness orsensory loss

Accumulation of tau, amyloid, neuritic bodies

(extracellular), neurofibrillary tangles(intracellular)

Presenilin 1: chromosome 14; age 30-50 onsetPresenilin 2: chromosome 1; age 30-65 onset

Amyloid Precursor ptn: chrm 21; age 40-60Apolipoptn E (e4 carriersmore amyloid plaques)

Neuritic bodies,

neurofibrillarytangles

Dementia with

Lewy Bodies (DLB)

Elderly Subcortical areas

and substantia

nigra

Dementia plus 2 of 3: parkinsonism,

hallucinations, or fluctuating

alertness/attn

Lewy bodies with α-synuclein and ubiquitin

Faster progression/shorter survival

Sensitive to anti-

psychotic meds

FrontotemporalLobar

Degeneration

Late-middle/elderly

Frontal andtemporal lobes

Similar to Alzheimer’sBehavioral changes most prominent ,

perseveration, decreased verbal

“knife-blade” like atrophy of frontal and temporallobe

Inclusion bodieswith tau fibrils in

neurons



(Pick’s disease) fluency

Huntington’s

Disease

30-50 years Caudate, putamen,

GP, cortex

Behavioral, cognitive changes and/or

movement dx, esp chorea

Gain of function of Huningtin gene CAG

expansion; extensive gliosis

atrophy of

caudate nucleus

w/ ventriculardilation

Wilson’s Disease (hepatolenticular

degeneration)

10-30 years Liver, brain, andeye

Liver dysfunctionMvmt dx (dystonia)

Behavior/cog changes

Inborn error of Cu metabolism accumulation ofCu in liver, brain, eye

Amyotrophic

Lateral Sclerosis

Middle-

aged/elderly

Ventral horns,

cortical atrophy inprecentral gyrus

Gradual weakness w/ no sensory

deficit

Degeneration of BOTH UMN/LMN. Neurogenic

atrophy

Spinocerebellar

Ataxias

Mean age: 11 Cerebellum Friedreich ataxia, hand clumsiness,

sensory deficits, progressive

deterioration

Trinucleotide expansion in intron

Prion diseases

Age of Onset Location of Lesions Clinical Features Gross/Microscopic Pathology Diagnostic Tests

Creutzfeldt-Jakob Disease

(CJD)

10%

inherited

Polymorphism at codon

129 with Val;

Rapidly progressive

dementia and startlemyoclonus (some ataxia)

Cortical atrophy and ventricular

dilation, spongiform encephalitis

CSF 14,3,3 protein

MRI changes

Familial Fatal Insomnia Polymorphism at codon

129 with Met

Insomnia Neuronal loss, and gliosis in specific thalamic nuclei and

inferior olivary nucleus

Variant Creutzfeldt-Jakob

Disease (vCJD)

Cortical plaques with surrounding halo of spongiform change; “mad cow disease”

Dementia and delirium

Disease Clinical Features Diagnosis Treatment

Delirium

Think: metabolic, toxic,

aseptic, increased ICP

Agitation, acute, inconsistent, fluctuating alertness,hallucinations, inattention

Widespread reduction in cerebral oxidative

metabolism; failure of cholinergic metabolism

Acute onset & fluctuating course,inattention, disorganized thinking, altered

LOC

Prevention, treat underlying illness, anti-psychotics, supportive care

Contraindications: benzodiazepines,

sedative-hypnotic, anti-cholinergics, drugs of parkinsonism, narcotic analgesics,

histamine-2-receptor blockers

Dementia

Think Alzheimer’s or

vascular dementia

Chronic, progressive, memory loss, alert/attn ok,

disorientation, constructional apraxia

Neuropathology: neurofibrillary

tangles/neuritic plaques in AD; lewy

bodies in PD/DLB; structural/functionalimaging, biomarkers (amyloid)

Vascular Dementia Focal motor, sensory, or reflex changes, sudden

and/or multi-stepwise decline; focal cognitive

impairments (visuospatial disturbance + aphasia)

Imaging: infarcts; ischemia Atypical Vascular Dementia: insidiously

progressive; not stepwise showing

extensive confluent white matter



abnormalities on T2 and FLAIR imaging

Normal Pressure

Hydrocephalus

Gait disorder, urinary incontinence, dementia

(triad); enlarged ventricles

70% respond to shunting

Dementia associated

with Movement

DisordersInfectious causes HIV-associated Dementia (HAD)

Can be somewhat reversible



Local Anesthetics

Drug Ester/Amide Potency Mechanism Topical Uses Parenteral Uses General uses Adverse Effects

Cocaine Ester-metabolized by

pl/hepatic

cholinesterases

Low Blocks voltage-gated Na

channels by

prolonging theirinactivationstate

Cation is activeform

Non-ionized

form cross into

m.

Laryngeal, nasalsurgery, UG

None Topical(lidocaine)

Infiltration

Nerve block &

field block

Spinal/Epidural

anesthesia

CNS: restlessness,dizziness, confusion,

circumoral paresthesis,

tinnitus, tremors, seizures

CV: bradycardia,

hypotension , heart block ,

cardiac arrest

Peripheral neurotoxicity,

hypersensitivity reactions,

ester typesPABA

(sensitizing)

Lidocaine Amide-

Weak bases;insoluble to

water

Metabolized by

liver P450

Intermediate Dermal (Shingles,

rash), laryngeal,oral (prevent

ventricular

arrhythmias)

Epidural,

infiltration, nerveblock , spinal

Bupivicaine High None Epidural,infiltration, nerve

block , spinal

Mepivicaine Intermediate None Epidural,

infiltration, nerve

block , spinal

Procaine(Novacain)

Low None Infiltration, nerveblock , spinal anes

Tetracaine

Epinephrine Adjunct for local

vasoconstriction;

Should not be used in areas

of end aa (“fingers, nose,penis and toes”) ears too…

General Analgesics

Drug Mechanism of Action Specific Actions Potency General uses Adverse Effects

Diethyl ether Correlation between lipid

solubility/potency

Potentiate GABA effects;

hyperpolarization &↓ excitability due to ↑ Cl-influx and K efflux

Stages:

I: analgesia

II: delirium

III: surgicalanalgesiaIV: meduallary

depression

Explosive, airway irritation, stable CV

response

Chloroform Arrhythmogenic, hepatotoxic, well

tolerated

Nitrous Oxide(laughing gas)

Loss of consciousness &analgesia due to

disruption of neuronal

firing & sensory

Fast induction andelimination

High MAC, notmetabolized

HypnosisHomeostasis

Analgesia

Amnesia

Autonomicinstability

Hypothermia

CardiacDesflurane Decrease vascular

resistance, not CO

MAC 6



Enflurane processing in thalamus

Reduced motor activity

due to inhibition ofneuronal firing in layer

IV of cerebral cortex

Decrease CO; produce

bronchodiliation

MAC 1.7 Muscle relaxation

”HHAAM”

Ketamine: traumavictims, sedation

of children;

coadmin w/benzodiazepine to

prevent deliriumand hallucinations

dysrhythmias

Nausea

VomitingDelirium

1/250000

estimateddeaths

Propofol

IV

Facilitate effects ofGABA at GABA-

Clionophore

Rapid emergence,less confusion

compared to

thiopental

Hypotension, respdepression, reduce

cerebral bld flow/

ICP ; not analgesic,not amnestic if

conscious,antiemetic

Midazolam

IV

Facilitate effects of

GABA

Produce amnesia

Less respiratory

depression than

propofol/thiopental,little effect on CVS

Unconsciousness

slower in onset,

longer thanthiopental

Ketamine Blocks NMDA receptors

Dissociative anesthesia

dream-like w/o loss of

consciousness

Cause analgesia, ↓sensory perception,

immobility and

amnesia

Increased HR, BP,

ICP and sympathetic

tone

ThiopentalIV

Lower MAC Produce CNS, resp,CV depression

The Ideal Anesthetic: potent, non-irritating, noninflammable, not toxic, not metabolized, not arrythmogenic, stable cardiovascular response, very slightly soluble in water,

quite soluble in oil, unable to trigger malignant hyperthermia, stable in soda/lime, not harmful to metal fittings, potent m relaxant

Anticonvulsants

Drug Mechanism of

Action

Metabolism Clinical Use Drug-Specific Adverse Effects Common Adverse

Effects

Phenytoin(Dilantin)

Na ch blockade Hepatic- P450system

Partial seizures,generalized seizures

Ataxia,nystagmus, drowsiness, lethargy,nausea, vomiting, rash, gingival hyperplasia,

blood dyscrasias

FatigueDizziness

Ataxia

DiplopiaNystagmusCarbamazepine(Tegretol)

Na ch blockade P450; induce ownmetab;

epoxidation to10,11-epoxide

Partial seizure; avoid in primary generalized

seizures

Dizziness, diplopia, nausea, ataxia, blurredvision, aplastic anemia, agranulocytosis,

thrombocytopenia, Stevens-Johnson syndrome

Oxcarbazepine

(Trileptal)

Na ch blockade Hepatic- induces

hepatic enzymes

Seizures Dizziness, nausea, headache, drowsiness,

ataxia, diplopia, fatigue, and nervousness;hyponatremia

Ethosuximide Inhibits T type Cach Absence seizures only Nausea, GI, anorexia, wt loss

Pregabalin

(Lyrica)

Unknown- potential

effect on α-2δRenal excretion Adjunct to partial

seizures

Confusion, edema, wt gain, typical side effects



subunit of Cach

Levetiracetam

(Keppra)

Unknown Renal excretion In combo with otherAED’s

Somnolence, fatigue, ataxia, behavioral

abnormalities; rare decrease in Hb& erythrocyte

count

Valproic acid

(Depakote)

Enhances GABA;

modulate VG Na ch,inh T type Cach

Hepatic-

Glucuronidation

Primarily generalized

epilepsy- 1st line

Nausea, tremor, sedation, confusion, wt gain,

hair loss, acute pancreatitis, bone mar sup,rash, hyperammonemia (“fat, bald, & shaky”)

Gabapentin

(Neurontin)

Enhance GAD; bindsα-2δ subunit of C ach

Renal excretion,

not metabolized

Partial seizures,

neuropathic pain

Somnolence, dizziness, nystagmus, ataxiz,

fatigue, weight gain

Lorazepam

Lamotrigine

(Lamictal)

Na ch blockade Hepatic-

Glucuronidation

Partial and generalized

seizures

Ataxia, dizziness, diplopia, N/V, Stevens

Johnson; 1% child/0.3% adults

Topiramate(Topamax)

Unknown Renal and hepaticelimination

Multiple seizure types Somnolence, dizziness, ataxia, difficulty w/memory, speech/langdysfxn, diplopia,

aggressive behave, anorexia, renal lithiasis

Zonisamide

(Zonegran)

Not completely

understood; T- type

Ca channels, Nachannels, carbonic

anhydrase inhibition

Renal excretion Adjunct tx for partial

seizures

Somnolence, ataxia, dizziness, fatigue, renal

lithiasis, anorexia

Phenobarbitol

Opioid Analgesics

Drug Synthesis

Or Distribution

Types Agonistic Action General uses Adverse Effects Actions Mediated

by Receptor

Subtypes

Endophins Arcuate nucleus &

ant. pit

Mu/delta receptors Analgesia:

mu, kappa, delta

Feeding:

mu/kappa/delta GI fxn: mu/kappa

Sedation: mu/kappa

Psychotomimesis:

Kappa

Diuresis: kappa Resp fxn: mu

Enkephalins Synthesized in small

interneuronsFound in

Periacqueductal

grey, lamina I/II

Leu-

Met-

Mu/delta receptors

Dynorphins Brain; often together

w enkephalins

A, B,

alpha-neo-

Kappa receptors

Morphine Papaversomniferum

Contraindications:

PharmacokineticsWell abs; high 1st pass

effect; conjugate to

Mu/kappa/deltaInhibit

adenylcyclase

Clinical Use: PAIN:post-operative, acute

MI, renal/biliary colic

CV: ↓ myocardial O2 demand,vasodilation, hypotension,

↑ICP



Major : head injuries,

seizures, alcohol

intoxication

Relative: asthma,

renal insufficieny,

history of opioidabuse, liver disease

glucuronide in

intestines/liver

Peak effect: 1 hr afterinj; duration: 3-4 hrs

hyperpolarization pain; chronic pain GI: constipation,↑ biliarysphincter tone/pressure,

nausea/vomitingGU: ↑ bladder sphincter tone,prolongation of labor, urinary

retentionOverdosestupor/coma,

respdep, miosis; tx w/naloxone

Withdrawal Effects:

Analgesia, euphoria

or dysphoria, inh of

cough reflex, miosis,physical dependence,

resp depression,

sedation

*w/o loss of

consciousness

Vomiting, chills,

fever, lacrimation,

diarrhea, rhinorrhea,seeking, craving

behavior

Occur after 8-12 hrs

of last dose

Meperidine 1/10th analgesic potency of morphine; poor oral abs; equivalent

respdep; miosis (mydriasis at toxic doses); high addiction liability ;short duration of action; metabolized to normeperidinerisk of

seizures

Resp depression, nausea,

vomiting, ↑ICP, posturalhypotension, constipation,

urinary retention, itching &

urticarial, restlessness,

tremulousness, hyperactivity

Occur after 3 hrs last

dose

Methadone Slightly more potent than morphine; less sedative &spasmogenic;

effective orally

Help wean off heroin

addict; maintain at40-100mg

Onset after 24-48

hrs last dose

Fentanyl 100x more potent than morphine as analgesic; given via IV & astransdermal patch

Patch: useful inchronic pain (3 days)

Oxycodone Use in combo w/ acetaminophen (7.5mg) or aspirin (5mg)

Buprenorphine

Codeine 1/10th analgesic potency of morphine; less constipation, lower

addiction liability , less sedation/respdep; used orally in combo w/

acetaminophen or aspirin for moderate pain; converted to

morphine by CYP 2D6

Antitussive

(suppress coughing)

NalbuphineParenteral only

Mixed opioid agonist (kappa)/antagonist(mu)

Naloxone

IV

Opioid receptor competitive antagonist (mu,

delta, and kappa)

Treats opioid

overdose; blocks

effects of morphineand other drugs

No dependence liability; all

others do; no constipation

Naltrexone

Oral

Opioid antagonist, mu, delta, kappa Used to prevent

relapse in chronic

alcoholics

Longer duration of

action than naloxone

Non-opioid Analgesic

Tramadol Synthetic codeine Weak mu agonist Mild to moderate pain Dry mouth, dizziness, sedation,



analog Inhibit uptake of NE and 5HT headache, seizures, abuse

potential-unclear

Drugs for Parkinson’s Disease

Drug Mechanism Notes Adverse EffectsLevodopa L-DOPA

(amino acid)

100-250mg, 3-4 times daily Nausea, orthostatic hypotension, hallucinations, dyskinesias

Less effective with foodHigh dose lead to dyskinesias (peak dose chorea, biphasic chorea, dystonia)

Carbidopa Works peripherally to block L-DOPA-DDC DA but cannot cross BBB; decrease symptoms in periphery, no CNS effects; does not effect

parkinsonism

Bromocriptine For PD, DA agonist at D2 receptors

Ropinirole Da agonists at D2 Longer duration of action,

but not as effective aslevodopa

Low standing BP, nausea, dyskenisa, hallucinations, sleepiness

Rare; lung & cardiac valve fibrosis, leg edema, compulsive behaviorsPramipexole

Selegiline MAO-B inhibitors

RasagilineEntacapone COMT inhibitor used in combo therapy

Amantadine Blocks NMDA, weak inducer of DA rel; can treat dyskinesias

Benztropine Anticholinergics; block mAch receptor; offsets the imbalance between Ach and DA

Apomorphine DA agonist at D1 and D2 receptors

Drugs for Multiple Sclerosis

Drug Type of Drug Mechanism of Action Adverse Effects

Interferone-beta Ag non-selective immunomodulators, proposed to act through inhibiting IFN-gamma activity

Glatiramer acetate Ag selective

Natalizumab

IV

Humanized monoclonalAb against cell adhesion

molecule alpha4-integrin

Reduce the ability of immune cells to cross BBB Progressive multifocal leukoencephalopathy

Antithrombotic agents

Clopidogrel Pro-drug, function

related to ADP receptoron platelet cell

membrane P2Y12

Irreversible inhibits P2Y12 receptor which is

important in platelet aggregation and cross-linking of fibrin by blocking the activation of

glycoprotein IIa/IIIb pathway; metabolized by

CYP2C19

Hemorrhage, neutropenia

Aspirin Irreversibly inhibits COX 1 GI ulcers, stomach bleeding, tinnitus

Drugs for Dementia



Donepezil Cholinesterase

inhibitors

Slows the breakdown of Ach by blocking

acetylcholinesteraselevels of Ach increase

Nausea, vomiting, loss of appetite, increased

frequency of bowel movements/diarrheaGalantamine

Rivastigmine

Memantine NMDA antagonist No evidence it can prevent or slow neurodegeneration

Drugs for Migraine

Sumatriptan Abortive for cluster andmigraine

5HT agonist; exerted in bile and urine4-6mg sc at onset for cluster H/A, poor bioavailability with oral administration, faster acting, but

with shorter duration with injection

Dihydroergotamine Abortive for cluster and

migraine

Act on 5HT receptors (agonistic)

vasoconstriction; inhibition of pro-inflammatory neuropeptide release

May increase BP, coronary artery vasopasm,

MI, ventricular fibrillation

Propanolol Prophylactic for migraine,β-adr blocker

Decrease frequency and severity of migraines Drowsiness, difficulty breathing, slowheartbeat, cold hands/feet, depression

Valproic acid Prophylactic for migraine, and cluster H/A, anti-convultant

Amitryptyline Prophylactic for migraine, tricyclic anti-depressant-inhibits 5HT/NE uptake Causes delirium

Topiramate Prophylactic for migraine and cluster, anti-convulsant

Know that the following classes of drugs can cause Delirium Anticholinergics, Opioids, Benzodiazepines, narcotic analgesics, sedative-hypnotic, histamine 2-receptor blockers

neurology domain guide

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