Neurology

Thursday, October 13, 2016

8:51 PM

1-Seizure Disorder
Sudden, excessive, and disorderly discharge of
cerebral neurons which causes abnormal movements
or perceptions
Peak incidence incidence in chilhood
Etiologies
Vascular
Infection
Trauma
Autoimmune
Metabolic
Idiopathic
Neoplasm
pSychiatric
Seizure Disorder: Classification
Partial seizures

Simple
Single locus in the brain
Focal motor or somatosensory symptoms
Consciousness is preserved

May be followed by transient neuro deficit (ToddsMay

be followed by transient neuro deficit (Todd s paralysis)
Complex partial
Impaired consciousness may be preceded,
accompanied, or followed by aura symptoms
Motor dysfunction: chewing movements, lip
smacking
Generalized seizures
Absence (petit mal)
Impaired consciousness
Mild clonic, tonic, or atonic components
Onset and termination abrupt, no post ictal
period
Myoclonic
No loss of consciousness
Single or multiple myoclonic jerks

 Tonic-clonic
Sudden loss of consciousness
Rigid, fall to ground
Urinary incontinence (common)
Post ictal

Status Epilepticus

Seizure lasting > 5 minutes or > 2 discrete

seizures without recovery of consciousness
Causes: antiepileptic therapy
discontinuation, medication noncompliance
BZDs, phenytoin (second line), phenobarbital
(third line)
Make sure to check a blood sugar

From <https://app.roshreview.com/exams/1054402>

2-Syncope

Syncope is defined as a sudden temporary loss of

consciousness with the inability to maintain
postural tone. It is a symptom with a wide variety of
life-threatening causes. Risk factors for
syncope include cerebrovascular disease, cardiac
manifestations, and hypertension. Despite
extensive workups, no cause for syncope is
found in approximately 50% of cases. When a
diagnosis is made, most causes of syncope are benign
and have favorable outcomes. Patients
with preexisting cardiovascular disease and
syncope from any cause are at the greatest shortand long-term risk of mortality. Syncope from
cardiovascular causes is associated with increased
mortality, whereas syncope due to neurocardiogenic,
orthostatic, and medication-related syncope is not
associated with increased mortality.

From <https://app.roshreview.com/exams/1084390>

Differentiate between syncope and

seizure
ECG for all
San Francisco Syncope Rule (high-risk
criteria): CHESS
o
CHF
o
Hematocrit <30%
o
ECG abnormal
o
SOB
o
Systolic BP <90 mm Hg
Adolescent athlete + syncope: HOCM
Young woman + abdominal pain + syncope:
ectopic pregnancy
Older male + abdominal/flank pain +
syncope: AAA
Sudden onset severe HA + syncope: SAH
Woman + prodrome of nausea, sweating,
warmth + syncope: vasovagal
Malignancy + sudden onset SOB + syncope:
PE

From <https://app.roshreview.com/exams/904320>

3- migrane HA

Migraine Headache

Gradual onset, unilateral > bilateral,

throbbing, pulsating
First episode: < 30 years old
F>M
Triggers: cheese, OCPs, pregnancy,
menstruation
Without aura: most common, N/V,
photophobia, phonophobia
Aura: scotoma, flashing lights, sounds
Abortive rx: triptans, DHE, antiemetics, NSAI
Ds
Ppx: Bs. CCBs, TCAs
Triptans, DHE: contraindicated in HTN or CV
disease

4-Tension Headache

Bilateral, band-like pain

NSAIDs

5-Cluster head ache

Cluster Headache

M>F
Sudden onset, unilateral repetitive brief HAs
Ipsilateral conjunctival injection, lacrimation,
rhinnorhea
Acute rx: O2

Cluster Headache

Patient will be a man

Complaining of sudden onset, unilateral,
repetitive brief HAs
PE will
show ipsilateral conjunctival injection, lacrimatio
n, rhinorrhea

Treatment is Acute: High flow

O2; Prophylaxis: CCB's

From <https://app.roshreview.com/exams/1054402>

6-TIA

Transient Ischemic Attack

Transient episode of neurological dysfunction

without acute infarction
10% of TIA patients will have a stroke within
90 days
Aspirin
+ dipyridamole or clopidogrel monotherapy
ABCD2 score: predicts likelihood of
subsequent stroke within 2 days

From <https://app.roshreview.com/exams/1054402>

7-Cerebral Vascular Accident (CVA)

History of atherosclerotic heart disease,
hypertension,diabetes, atrial fibrillation
Sudden onset neurologic complaint
Focal weakness, sensory abnormalities, visual
changes, language defect, altered mentation
Deficits >24 hours Deficits >24 hours
If <24 hours, transient ischemic attack (TIA)
Etiology CVA
Principal mechanisms
Large artery thrombosis
Small artery thrombosis (lacunar)
Embolic (cardiogenic or artery-to-artery)
Vascular dissection
Systemic hypertension
Bleeding

Risk factors
Age

 Family history
Diabetes
Hypertension
Smoking
Hypercholesterolemia
Atrial fibrillation

Laboratory Evaluation
Physical exam
Neuro exam
Cardiac/carotids
Labs
Non-contrast CT scan
CBC, sedimentation rate, electrolytes, glucoseC
C, sed e tat o ate, e ect o ytes, g ucose
VDRL, lipid profile, coagulation panel, thyroid
function

Treatment
Modify risk factors
Anti-platelet agents
Aspirin is first-line therapy; add dipyridamole or
clopidogrel
Anticoagulation therapy
Heparin for those with risk for recurrent stroke
(A fib,stroke in evolution) Silth
Surgical therapy
Carotid endarterectomy
Thrombolysis
Tissue plasminogen activator within 3 hours
Rehabilitation

8-Intracranial Mass Lesion

Brain neoplasms are a diverse group of primary
tumors
Glioblastoma
Is most common primary in adults

 Symptoms and signs depend on size, growth

and location of tumor
Most frequent are headache, seizure, and signs of
increased intracranial pressure (mental status
changeincreased intracranial pressure (mental status
change, vomiting, papilledema)
Diagnose with CT/MRI and biopsy
PET scan may be helpful
Treatment
Surgery, RT, chemotherapy

9- Essential Tremor
Cause is uncertain
Sometimes inherited autosomal dominant
Begins at any age; typical onset age 60s
Involves hands and/or head
Lacks hypokinetic features and rigidity of
Parkinsons disease
Alcohol improves tremor

 Treatment
Propranolol

10-Parkinsons Disease
Idiopathic, slowly progressive, degenerative CNS
disorder due to dopamine depletion in basal ganglia
Insidious onset in older patient
Men > women
Clinical
Pill-rolling tremor, rigidity, bradykinesia, postural
instability, micrographiamicrographia
Physical exam
Mask-like facies, cog wheeling of extremities,
DTR normal, shuffling gait, may have intellectual
deterioration
Dementia (50%) and depression common
Parkinsons Disease

Lewy bodies, substantia nigra dopaminergic

neuron loss
TRAP: Tremor (resting, pill
rolling), Rigidity, Akinesia, Postural instability
Carbidopa/levodopa, anticholinergic drugs

Avoid antipsychotics

11-Multiple Sclerosis
Slowly progressive CNS disease with disseminated
patches of demyelination in brain and spinal cord
Probably autoimmune in nature
Women > men; onset age <50; Northern European
descent
Episodic symptomspyp
Sensory abnormalities, blurred vision (optic
neuritis), sphincter disturbances, weakness (heat
may worsen symptoms)
Lhermittes sign positive (sensation of electricity
down back with passive flexion of the neck)
Fatigue, depression, bladder urgency, weakness,
impaired coordination
Laboratory Diagnosis

 CSF studies
Mononuclear cell pleocytosis
Elevated levels of total Ig
--Presence of oligoclonal Presence of oligoclonal
IgG
MRI
Abnormal hyperintense areas in white matter, found
in brainstem, cerebellum, spinal cord
Treatment
Relieve symptoms
Modify disease course
Corticosteroids
Interferon-1b (Betaseron), IFN-1a
(Avonex), IFN-1a (Rebif)
Glatiramer acetate (Copaxone)
Natalizumab (Tysabri)Natalizumab (Tysabri)
Note: All of the above for relapsing, remitting MS
Mitoxantrone (Novantrone) (for worsening
forms of MS and secondary progressive MS)
IV gamma globulins

12-Meningitis
Inflammation or infection of the meninges
Bacterial
Signs and symptoms
Headache, nuchal rigidity, fever, change in
mental status,seizures
Brudzinski or Kernig sign
Rash: petechial, think Neisseria
Labs
CSF
Rapid antigen tests

Cryptococcal Meningitis

HIV, CD4 < 100

Meningismus uncommon
Rx: amphoteracin B + flucytosine

From <https://app.roshreview.com/exams/1055428>

13-Encephalitis

Infection of the brain parenchyma

Causes include herpes (#1), enterovirus, EBV, CMV,
measles, Eastern and Western equine, St.
Louis,varicella, West Nile
Physical exam
Fever, malaise, stiff neck, nausea, altered
mentation

 Signs of upper motor neuron lesion

(exaggerated DTRs, spastic paralysis)
Labs
CSF: lymphocytes; glucose normal or
decreased; protein
Polymerase chain reaction
Encephalitis
Treatment
Supportive (acetaminophen)
Acyclovir: Herpes simplex, varicella-zost
Ganciclovir or foscarnet: CMV
Avoid steroids

14-coma

15-Myasthenia Gravis
Due to block of neuromuscular transmission due to
auto immune antibodies against ACH---> cause
progressive weakness
Acetylcholine receptors
Antibody-mediated autoimmune
Fluctuating weakness/fatigue of voluntary muscles
Proximal muscles affected more than distal
Diplopia, dysphagia, ptosis,( eyelid weakness more
prominent with upward gaze) facial weakness,
difficulty swallowing
Early stage affects the eye muscles; activity
increases weakness
All ages affected; mainly young women

Diagnosis
Acetylcholine-receptor antibodies (8990%)
Short-acting anticholinesterase (Tensilon test:
edrophonium) ( rapid response to IV
edrophonium pg 355 pearls)

Improvement in weakness
Cholinergic side effects: nausea,
diarrhea, bradycardia

EMG
-Ice pack test--> place ice in the eye lid for 10
min--> ocular myasthenia ( ptosis improves with
cold)
Treatment
Anticholinesterase drugs (pyridostigmine or
neostigmine)
Thymectomy
Plasmapheresis to relieve symptoms
Corticosteroids (long-term treatment)
Aminoglycosides worsen disease so should be
avoided

Myasthenia Gravis

Autoimmune destruction of Ach receptors

Proximal muscle weakness, ptosis, diplopia
Sx with activity
Myasthenic crisis: acute respiratory
compromise
Ice test: sx ( sx decrease with cooling)
Edrophonium: sx in myasthenic crisis
and sx in cholinergic crisis

ice test. When ptosis is present, an ice pack is

placed over the affected eye for two minutes, and
the ptosis resolves.

16-Temporal artheritis

Temporal arteritis is a chronic segmental

vasculitis of medium and large vessels. Although

it most commonly affects one or more branches of the

carotid artery (temporal artery, ophthalmic artery, and
posterior ciliary artery), the aorta can also be
involved. Aortic involvement can lead to valvular
insufficiency, aortic arch syndrome, and
dissection. The carotid and vertebrobasilar arteries
can also be affected, which can lead to neurologic
complications. The condition is associated with a
markedly elevated erythrocyte sedimentation rate (50
100 mm/hr).

From <https://app.roshreview.com/exams/1084390>

Temporal Arteritis (Giant Cell Arteritis)

Patient will be a women > 50 y/o

Complaining of monocular visual loss,
unilateral headache, jaw claudication
PE will show tender temporal Artery
Labs will show ESR > 50
Diagnosis is made by temporal artery biopsy
Treatment is high dose steroids
immediately on suspicion
Comments:
Associated polymyalgia rheumatica

From
<https://app.roshreview.com/exams/953672/review?
type=incorrect>

Temporal Arteritis

Elderly females
Unilateral temporal HA, jaw claudication
Ophthalmic artery occlusion
irreversible blindness
PMR
ESR, CRP
Dx: temporal artery biopsy
Immediate high-dose steroids

Giant Cell Arteritis

Granulomatous vasculitis of the temporal artery
Etiology unknown
Typically ages
May coexist with polymyalgia rheumatica
Clinical
Headache, jaw claudication, vision loss Fever, fatigue,
weight loss
Physical examination
Temporal artery tender, enlarged, and erythema
Labs
Elevated sedimentation rate, anemia, leukocytosis
Sedimentation rate 50 mm/hr
Diagnosis
Artery biopsy
Treatment
Corticosteroids

Temporal artery tenderness, jaw claudication,

and low-grade fever in a 75-year-old woman,
strongly suggestsgiant cell (temporal)
arteritis (GCA). GCA is a vasculitis primarily of large
and medium-sized vessels and is the most common
systemic vasculitis. The recommended initial
treatment for patients presenting with GCA (without
signs of ischemic organ damage, eg, visual loss) is
glucocorticoid therapy with prednisone (40-60 mg
single dose).

Vasculitis

Temporal arteritis: PMR, carotid artery

branches affected, vision loss, Rx: immediate
steroids
Takayasus arteritis: Asian, decreased pulses
PAN: generalized without lung
involvement, HBV
Buerger's disease: smokers, claudication of
hands/feet
Granulomatosis with polyangiitis (GPA): Uppe
r and lower respiratory sx + renal sx, c-anca
Microscopic polyangitis: similar to GPA but
without nasopharyngeal involvement, p-ANCA
Churg-Strauss syndrome: vasculitis + eosino
philia + asthma
Cryoglobulinemia: HCV, malaise, skin lesions,
joint pain
Behet's disease: oral and genital
ulcers, hyperreactivity to needle sticks

From <https://app.roshreview.com/exams/904320>

From
<https://app.roshreview.com/exams/953672/review?
type=incorrect>

17-Bells Palsy
Idiopathic facial paresis of lower motor neuron type
May be link to recent viral infection: herpes
simplex or varicella-zoster virus

 Inflammatory reaction involving facial nerve (CN VII)

near stylomastoid foramen
Clinical
Hemifacial weakness
Difficulty closing eye
Ipsilateral ear pain

PE
Seventh nerve palsy
Taste loss anterior 2/3 of tongue
Hyperacusis
Management
60% resolve without treatment
Corticosteroids may be considered

Bells Palsy

Most common cause: HSV

Unilateral facial nerve paralysis
Bilateral: Lyme disease, infectious
mononucleosis
CN VII
Viral prodrome

No forehead sparing
Postauricular pain
Taste disturbance
Hyperacusis
Prednisone, artificial tears, tape eyelid shut

18-Guillain-Barre syndrome (GBS)

Pearls pg 354

GuillainBarr Syndrome
Demyelinating injury
Associated with viral infection, stress,
Campylobacter jejuni enteritis

 Progressive, ascending, symmetric weakness with

variable paresthesia or dysesthesia
Physical exam
DTRs, weakness in ascending pattern
Loss of proprioception
Labs DX
Spinal tap: total protein with normal WBC
cell count
EMG: consistent with demyelination

Treatment
Watch for involvement of respiratory muscles
IV immunoglobulin
Plasma exchange
Steroids are not effective

Guillain-Barre syndrome (GBS) is a symmetric,

progressive ascending muscle weakness that
usually starts in the legs and may be acute or
subacute. The condition is life-threatening if
respiratory or swallowing muscles are involved. GBS
can follow minor respiratory or GI illness,

inoculation, or surgical procedures. It carries a poorer

prognosis when it follows Campylobacter jejuni
infection. The clinical hallmark of GBS is lack of
deep tendon reflexes. Patients experience weakness
of >2 limbs that typically begins with the proximal
lower extremities. As weakness progresses, patients
may experience shortness of breath, constipation,
facial weakness, dysphagia, ophthalmoplegia,
dysarthria. And sensory disturbances. Lumbar
puncture results will demonstrate increased CSF
protein but a normal cell count. Treatment is
supportive. Plasmapheresis or IVIG may improve
recovery time and decrease residual neurologic
effects.

From <https://app.roshreview.com/exams/766598>

Guillain-Barr Syndrome

Antecedent pulmonary or GI illness

(Campylobacter jejuni)
Rapid ascending symmetrical weakness
Lower extremity weakness > upper
extremity weakness
Deep tendon reflex loss respiratory failure
Normal rectal tone
CSF: markedly protein with up to 100
lymphocytes/L
Obtain pulmonary function tests
Rx: IVIG or plasmapharesis, possible
prophylactic intubation

15- Myastenia gravis

Myasthenia Gravis
Due to block of neuromuscular transmission
acetylcholine receptors

Fluctuating weakness/fatigue of voluntary muscles

--- Proximal muscles more affected
Diplopia. dysphagia, ptosis, facial weakness, difficulty
swallowing
Early stage affects eye muscles, activity increases
weakness

All ages affected; mainly young women

19-Hunghtington dz

Huntingtons Chorea
Autosomal dominant
Onset ages 3055, with gradual chorea and
dementia
Personality changes, impulsiveness, aggressive
behavior, depression, and paranoid psychosis are
noted (may precede the motor manifestations)
Motor manifestations
Flicking movements of the extremities
Lilting gait
Inability to sustain a motor act
Facial grimacing
Ataxia

 Dystonia
Progressive
Labs
CSF normal
CT scan: cerebral atrophy
Diagnosis by genetic testing
Treatment
Supportive only
Genetic counseling
Anti-dopaminergic agents (haloperidol) may
work early
Fatal 1520 years after diagnosis

20-Cerebral Aneurysm
Asymptomatic until expansion or rupture
Symptoms vary depending on site
Rupture characterized by sudden, severe headache,
altered mental status, photophobia, vomiting
Focal neuro signs (unusual)
CT, MRA, or angiography
Treatment
Nimodipine
Surgery

21-Simple Concussion

 Transient loss of consciousness followed by complete

recovery
Implies an injury which resolves 710 days
without complications
Clinical
Headache, dizziness, nausea/vomiting,
sleepiness
Short period of amnesia is often related
No focal neurologic findings
Brain contusion Brain contusion
Brain damage with prolonged coma, amnesia, &
focal signs
May suffer from chronic impairment
Treatment: monitor for return to activity
Complications- Post-concussion syndrome
Presents immediately or months after injury with
headache, dizziness, sensitivity to light or noise,
blurred vision, irritability, anxiety, depression, or
change in personality

22-Delirium

Sudden onset, fluctuation

Impaired speech
Impaired orientation
Disorganized thinking

Hallucinations

23-Dementia

Gradual loss of mental capacity

Preserved attention, motor function, speech
Irreversible causes: Alzheimers, vascular
dementia, Creutzfeldt-Jakob disease
Reversible causes: depression, B12 deficiency,
syphilis, hypothyroidism, NPH, drug use, intracranial
mass

24-Peripheral Neuropathies

Sciatic: buttock injury, hip dislocation,

knee flexion, foot drop, rx: ankle splint
Common peroneal: proximal fibula
injury, footdrop, rx: ankle splint
Radial: crutches, wrist/finger drop, rx: wrist
splint
Ulnar: elbow injury, finger
adduction/thumb grasp, 4th/5th digit paresthesias
Lateral femoral cutaneous: inguinal
ligament entrapment, upper
thigh dysesthesia/numbness

From <https://app.roshreview.com/exams/1054402>

25-Reflex Sympathetic Dystrophy (Complex

Regional Pain Syndrome)

Patient with previous extremity injury

Light touch extreme pain
Rx: NSAIDs, gabapentin, sympathectomy

From <https://app.roshreview.com/exams/1054402>

Complex regional pain syndrome (CRPS) is not

commonly encountered in primary care. However,
CRPS presents with profound signs and symptoms.
CRPS-1 occurs after a noxious neurological event, such
as soft tissue crush injury, immobilization, orthopedic
surgery and podiatric surgery. Any insult to the
integrity of peripheral nerves is a possible etiology.
This condition is felt to be due to activation of
peripheral nociceptors, causing an increase in
neuroexcitatory agents in the spinal cord, leading to
upregulation and sensitization of peripheral and
central pain pathways. Lowered neuronal thresholds
result in over activity and dysregulation of the
sympathetic nervous system. The most common
presenting symptoms include: neuropathic pain
(spontaneous, burning, dysesthetic, diffuse), allodynia
(pain felt from a nonpainful stimulus, such as clothes
or bed sheets on the skin), hyperesthesia
(exaggerated pain response to a painful stimulus),
hypoesthesia (decreased sensation/numbness in a
painful area), hyperpathia (continued sensation after a
stimulus is removed, such as continuing to feel

vibration after a tuning fork is removed), decreased

range-of-motion and joint guarding, skin changes
(edema, erythema, temperature alterations, changes
in hair growth and nail composition) and motor
impairment. A classic presentation is post-surgical
patients with days-to-weeks onset of distal
extremity diffuse neuropathic pain, edema and
erythema, as in the above patient. Most patients are
treated with a mix of medication options:
corticosteroid burst, intranasal calcitonin, NSAIDs,
short course of opioids, gabapentin, tricyclic
antidepressants and transdermal clonidine or
lidocaine.

Subdural
Hematoma

-Usually due
to tearing of
bridging veins
on brain
surface to
dorsal sinuses
-Can also
occur from
arterial
rupture

Signs &
Symptoms
-HA, vomiting,
dysphagia,
anisocoria, CN
palsies, nuchal
rigidity, ataxia
-H/o
acceleration/decele
ration injury

Workup

Manag

-Noncontrast head CT
will show crescentshaped hematoma
because it extends
beyond the suture lines

-ABCs a

-C-spin

-Shorthypove
to pC
cerebra
vasoco

-Usually acute but

can become
chronic

-Manni
saline t

-Seizur
-Behavioral
changes such as
apathy, cognitive
impairment with
chronic SDH

-May re

-ICU ad
serial h

Progn

-More s
epidura
those r
is 40-6

rosh
Subdural Hematoma

Patient will be elderly or alcoholic

With a history of a fall or traumatic head
injury

Complaining of headache, mental status

changes, seizures, or focal deficits

Diagnosis is made by non-contrast CT,

crescent-shaped hematoma
Most commonly caused by rupture of the
bridging veins
Treatment is neurosurgical consultation

***The textbook presentation of an epidural

hematoma is that there will be a lucid interval
followed by a loss of consciousness, however in reality
EITHER a subdural or an epidural can have a lucid
interval LOC; the only difference is that the
decompensation to coma may be slower in a
subdural

Subdural Hematoma

Epidural Hematoma

Subarachnoid
(Stroke)

Epidural Hematoma

-Due to tearing of middle meningeal

artery

Signs &
Symptoms

-Rarely seen in kids < 2 and in the

elderly as the dura is firmly attached in
these ages

-HA, vomiting,
confusion/lethargy
, aphasia, seizures,
hemiparesis

Workup

Noncontr
head CT
shows
hematom
that does
-Unconsciousness, not cross
suture lin
abnormal pupil
brain
reactions to light,
parenchy
or abnormal
a may be
posturing due to
compression of CN compress
to the
by hematoma
midline
-Usually coexists
with a skull
fracture

Subdural Hematoma

Patient will be elderly or alcoholic

With a history of a fall or traumatic head
injury
Complaining of headache, mental status
changes, seizures, or focal deficits
Diagnosis is made by non-contrast CT,
crescent-shaped hematoma
Most commonly caused by rupture of the
bridging veins
Treatment is neurosurgical consultation

From <https://app.roshreview.com/exams/1049990>

Subarachnoid Hemorrhage
Spontaneous arterial bleeding into
subarachnoid space
May result from an aneurysm
Associated with connective tissue disease
Head trauma as a cause is rare
Abrupt onset
Worsens over 3090 min
Causes headache, stiff neck, photophobia, and
papilledema
Blood in spinal tap

 Treatment
Nimodipine reduces risk of stroke
Surgical clipping

Subarachnoid Hemorrhage

Sudden onset, thunderclap headache

Ruptured berry aneurysm
Polycystic kidney disease
Head CT/LP
Xanthochromia
Nimodipine

From <https://app.roshreview.com/exams/1054402>