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284 Cards in this Set

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Headache Causes:
_________ nerve endings on extracranial structures that produce referred pain to the head when stimulated

Pain stimuli from brain tissue above the tentorium conveyed by the _______ nerve

Pain impulses from posterior fossa conveyed by glossopharyngeal, vagus, and first two cervical nerves
Nociceptive

trigeminal
Headache Evaluation:
Must distinguish benign headache from serious or ________ headache
________ helps decide which patients may have benign pain or pain associated with major intracranial lesion
malignant

History
Headache History:
_______,________,________,________

Exacerbating and relieving maneuvers

Ominous sign: acute onset of worst headache of his/her life (___________)
Suggests ______________
Quality, location, duration, course

Thunderclap HA

subarachnoid hemorrhage (SAH)
________:
throbbing, pressure, jabbing, vice like

Location:
Especially if pain is __________ in origin - temporal location and temporal arteritis
___________ pain is occipitocervical occasionally associated with retro-orbital pain (unilateral)
Multifocal pain is usually a ________ etiology
Quality

extracranial

Posterior fossa

benign
________: Menses, food, caffeine, alcohol, stress

____________: Worse in morning or awakening from sleep may mean increased intracranial pressure or sleep apnea

Associated symptoms: _________ disturbances, nausea, vomiting, nasal congestion, hay fever

Other: medications, (especially _________ and OTC meds), family history, past medical history
Triggers

Diurnal variations

Visual

analgesics
Physical Exam in Acute Headache:
Vital signs, neuro exam, _____ testing, _________ exam

Fever: must r/o _________ irritation with Kernig’s and Brudzinski’s

Always check ____, besides headache from HTN, can also be present with headaches from -
Intracranial hemorrhage, preeclampsia, pheochromocytoma
vision

fundoscopic

meningeal

BP
Eye exam:
Visual _______ decreased in glaucoma, temporal arteritis, and optic neuritis
Visual ______ problems in venous sinus thrombosis, tumor, or aneurysm
__________ defects in intracranial masses or optic neuritis
Ptosis and meiosis (__________) with acute headache can signify ___________
Papilledema or absent venous pulsations can signify increased __________
acuity

fields

Pupillary

Horner’s syndrome

corotid artery dissection

intracranial pressure
Physical Exam:
Complete neurologic evaluation and mental status exam is mandatory

Neuro exam:
Motor and sensory systems, gait and cerebellar functions, ________ drift
Any abnormality on mental status or neuro exam warrants emergent __________
pronator

neuroimaging
CT or MRI with:
________ headache in previously well patient, _________ headache disorder, new onset headache in mid or later life, headaches with focal neuro sx, headaches that disturb ______

CT or MRI, and CSF exam with:
_________ irritation or impairment of _________
_____ or meningeal infection
Severe

progressive

sleep

Meningeal

conciousness

SAH
Patient complaints:
Poor concentration and other vague complaints
constant daily headaches, vise like, tight hat band
Worse with stress, fatigue, noise and glare
Most intense in neck and back of head
No focal neuro sx
Tension HA
Tension headache Treatment

If simple ________ not effective, try anti migrainous meds

Relaxation techniques: Hot baths, massage, biofeedback

Look for underlying cause of ________
analgesia

anxiety
Episodic headache disorder with various combinations of neuro, GI, and autonomic changes with dx based on headaches characteristics and associated sx.
PE and lab usually normal

15% in women and 7% in men
May begin at any age from early childhood on
peaks in adolescence and early adulthood
Migraine HA
Migraine Headaches Types:

_____ migraine -
Migraine without aura

______ migraine -
Migraine with aura

_____ -
Focal neuro sx (visual) that precede the headache
Common

Classic

Aura
Symptoms:
Usually pulsating, unilateral, __________ pain
With nausea, anorexia, and sometimes vomiting
__________,__________, and occasionally osmophobia
Diagnosis or migraine requires at lease one of the above, especially if no _____ sx
frontotemporal

Photophobia, phonophobia

GI
Migraine Headaches Symptoms:
In children may have __________ pain, sleep disturbance, and motion sickness

Onset over age ___ rare, but can have recurrence of migraine that was in remission

Can have transient hemiparalysis or hemiplegia in genetic migraines called ______________
abdominal

50

familial hemiplegic migraines
Familial hemiplegic migraines:
Attacks with major neuro sx

Migraine with hemiplegia or ________
Dysfunction outlasts the headache by ___________
coma

hours or 1-2 days
Migraine Headaches Etiology:
_______(65-91% have family hx)
CNS susceptibility to certain stimuli (foods, alcohol)
________ factors
Sequential neurovascular events
Genetic

Hormonal
Goals of Treatment:
Treatment of _________
_________ of recurrent headaches

Patient information -
Tell patient they have migraines
Explain that this is a _______ condition
Help them understand their role in the treatment process
Explain the importance of a headache ________
acute attack

Prevention

benign

diary
Treatment Acute migraine:
May be relieved with single agent or combination of agents
_________ modification therapy is important

Some attacks respond to simple analgesics -
Acetamenophin, ASA, NSAIDS (_______)
_______ have little use in migraine therapy
Overuse of analgesics is common in migraineurs, so monitoring amount of analgesics is important
_________ for nausea (also slight sedative effect is beneficial)
Behavior

Toradol

Opoids

Antiemetics
Treatment Acute migraine:
“Migraine specific” _______ agonists -
5HT1 receptor agonists
Effective in alleviating migraines
Patients must be instructed in appropriate usage
Sumatriptan (Imitrex)
Naratriptan (Amerge)
Rizatriptan (Maxalt)
Frovatriptan (Frova)
seratonin
Migraine prevention:
Drugs used should be limited to patients who have
More than ___ migraines/month
Are willing to take _____ meds
Adequate trial period should be given, using adequate dosages, before it is considered ineffective
4

daily
___________ migraine (rare):
Blindness or visual disturbances in both visual fields followed by
Dysarthria, disequalibrium, tinnitis
Perioral and distal paresthesias
Transient loss or impairment of consciousness or confusional state
All followed by throbbing occipital headache with nausea and vomiting
Basilar artery
___________ migraine:
Lateralized pain about the eye
N and V, diploplia
Transient opthalmoplegia of 3rd and 6th nerve may outlast pain for weeks
Very rare type of migraine
Opthalmoplegic
_______ Headache: Is a group of symptoms with specific course
Less than 10% of all headache sufferers
More common in men, and onset later in life than migraines
Rarely in childhood, and less often a family hx than migraines
Cluster
Cluster Headache Symptoms:
Pain is extreme
Steady, nonthrobbing, retro-orbital on one side of head, may spread to ________ side of face and neck
Attacks awake patients 2-3 hours after sleep onset, not relieved by dark quiet area
Congestion of ________ and injection of _________ on side of headache (with occasional tearing)
________ on ipsilateral side of the face and forehead
May be signs of Horners syndrome (ptosis, meiosis)
ipsilateral

nasal mucosa

conjunctivae

Sweating
Cluster Headache Symptoms:
Named cluster because symptoms frequently occur over days or weeks with headache free periods of several months to years
Very susceptable to _______ as a precipitant, even small amounts
Etiology of clusters unknown, but pain distribution suggests _________ nerve dysfunction
alcohol

trigiminal
Cluster Headache Treatment: Abortive (acute headaches) or prophylactic to prevent headaches
May respond to ___ by mask 7-10 L/min for 15 min
Effective in 70% of patients within several minutes
Preventative medicine -
________, divalporex sodium, _________ (CCB), methysergide (sansert), corticosteroids
O2

Lithium

verapamil
Headaches of structural brain disease:
Manifestation of underlying brain disease
Seen in ________, TIA’s, intracerebral and subarachnoid hemorrhage
Infection seen in _________ - Neck stiffness, + Brudzinski’s and Kernig’s

HA from sinusitis, brain tumors, & SAH
infarction

meningitis
Headaches from _________:
Most prominent feature of sinusitis
Dull, aching, and non pulsatile
Exacerbated by movement, cough, and straining.
Improved with decongestants
Worse on awakening from prolonged lying down, improved with prolonged standing
Sinusitis
Headaches from sinusitis

Pain location depends on sinus involved
_________: ear, face, dental
_______: behind eyes, vertex of skull with tenderness to undersurface of supraorbital rim
________: between or behind eyes, radiating to temples
________: pain to vertex or orbit

_______sinusitis: seldom a cause of headaches
Maxillary

Frontal

Ethmoid

Spenoid

Chronic
Brain Tumors

Posterior fossa: headaches especially with __________ if obstuction of CSF occurs

Supratentorial tumors less likely to cause headaches but more frequently cause _______, focal defects or altered mental status

Increased ____________ does not produce distortion of pain sensitive structures, but headache is from whatever has caused the increased pressure
hydrocephalus

seizures

intracranial pressure
Brain tumors (Intracranial Mass Lesions):
Usually due to displacement of vascular structures
Posterior fossa cause ________ pain
Supratentorial cause ______
Findings are too inconsistant and nonspecific in character
Signs of focal diffuse _____________ or increased IC pressure warrants further investigation
_________ headache, or new onset in middle or later life requires work up
occipital

bifrontal

cerebral dysfunction

Progressive
causes 5-10% of strokes Usually due to aneurysm or AVM rupture
No cause found in 20% of cases
Subarachnoid Hemorrhage (SAH)
SAH:
Sudden onset headache (worst I’ve ever had/____________)
Nausea and vomiting
Loss or impairment of conciousness which can progress to ______
Confused irritable patient if conciousness is regained with sx of altered mental status
_______ rigidity
Focal neurologic deficit may suggest site of underlying lesion
thunderclap headache

coma

Nuchal
SAH Imaging:
_____ Immediately
Preferable to MRI in 1st 24 hours
If CT normal with strong suspicion of SAH, must do ________ for blood to R/O SAH
Once patient stabilized, may do ___________ to localize source of bleeding and consider for surgery
Need bilateral carotid and vertebral angiography because aneurysms can be multiple
CT

CSF exam

angiography
SAH TX:
Measures for comatose patients
Concious patients confined to bed and advised against straining and exertion
_________ treatment for headache and anxiety
_________ and stool softners
Gradual lowering of ____ if hypertensive but not below diastolic BP of 100mm/hg
________ to prevent seizures
_________ management of AV malformations and aneurysms
Symptomatic

Laxatives

BP

Phenytoin

Operative
Distinguished from other headaches because of the shortness of the attacks
(1-2 seconds or less) & the distribution of the pain (along affected nerve root)

Usually responsive to treatment with __________ such as phenytoin, carbamazepine, gabapentin, and occasionally baclofen
Cranial Neuralgias

anticonvulsants
_________ neuralgia (tic douloureau):
Stabbing (lancinating), spasmotic, severe pain in one of the divisions of the trigeminal nerve
Lasts only seconds
Occurs many times/day for weeks at a time
Usually provoked by slight _____ to the face such as the lips or gums
Small minority of cases associated with ___________, cerebellopontine tumors, aneurysms, ______
Unlike true trigeminal neuralgia, those that are associated with theses conditions have objective findings of neurologic defects
Ex: areas of diminished _________
Trigeminal

touch

multiple sclerosis

AVMs

sensation
Trigeminal neuralgia:
Can be life threatening if it interferes with _______

Treatment:
Medical with meds such as __________
If unsuccessful medical treatment, surgical microvascular decompression and/or radiofrequency lesioning of the medial portion of the trigeminal nerve
eating

carbamazepine
_____________ Neuralgia:
Rare and much less common than trigeminal neuralgia
Severe stabbing pain from throat to ear
Initiated by stimulation of trigger zones such as post pharyngeal wall, swallowing, yawning and/or coughing
Treatment is surgical microvascular decompression as medical treatment is ineffective
Glossopharyngeal
Postherpetic Neuralgia:
1/3 of the cases of _________ produces head pain due to cranial nerve involvement
Sometimes, persistant severe burning pain follows the initial illness
It may resolve in weeks, or persist from months to years (especially in the ________)
Herpes zoster

elderly
Herpetic Neuralgia:
Localized over the distribution of the cranial nerve, and patients experience severe tenderness even with light touch
Most frequent nerve involved is the ____ division of the trigeminal nerve (_________)
Geniculate herpes is the ____ nerve and involves pain in the external auditory canal and the pinna
_________ syndrome is facial paralysis with geniculate herpes
1st

opthalmic herpes

7th

Ramsay Hunt
Occipital neuralgia:
Occipital pain starting at the base of the skull and provoked by neck _______
Tenderness in the region of the occiput and altered sensation in the ____ dermatome

Treatment:
Soft collar, muscle relaxants, PT, injections of ________, NSAIDS
extension

C2

analgesics
Headache Due to ____________:
Superficial temporal, vertebral, ciliary, and opthalmic arteries are most severely affected

Clinical findings:
Usually elderly patient
Headache with myalgias, malaise, anorexia, weight loss
Loss of _______ is the worst and most feared manifestation of this illness
Occurs commonly
Giant Cell (temporal) arteritis

vision
Headache Due to Giant Cell (temporal) arteritis:

Physical exam -
_________ over scalp and temporal arteries

Treatment -
________ 60mg/day at 1st sign
Temporal artery ______ immediately
Low dose ____ to prevent stroke
ESR and patient sx should dictate taper of prednisone
____________ are 17 times more likely in patients with giant cell arteritis
Tenderness

Prednisone

biopsy

ASA

Thoracic aortic aneurysms
Neurologic Exam and Diagnostic Testing: Neuro Hx

Location, quality, and timing of sx
PMH, Social Hx

Pain generally is due to _________ nervous system problems where aphasia means abnormality of ___

sensory and motor loss means large lesion in the _______ or smaller lesion lower down on the neuraxis

Small lesions in spinal cord and brain stem can cause significant neuro problems, where small lesions elsewhere may be ____
peripheral

CNS

cortex

asx
Neurologic Exam and Diagnostic Testing: Neuro Hx

Some sx result from lesions at several levels of the nervous system
Ex: double vision from _____ lesions
Brain stem
Peripheral nerves
Neuromuscular jct
EOM’s

Double vision from non focal problems
Increased __________
focal

intracranial pressure
Pace and order of symptoms:

__________ diseases are gradual
Alzheimers, Huntingtons, Parkinsons

_________ diseases are rapid
Stroke, SAH
Degenerative

Vascular
Examination Approach: injury is from one of two possibilities:

_________ pathway structure is disrupted

_______ to pathway is disrupted
Final common

Input
In the _______ system the final common pathway includes:
Anterior horn cells
Nerve
Neuromuscular junction
Muscle itself
Injury results in dysfunction of the muscle
If the efforts to stimulate the final common pathway fail, clinician can conclude the lesion is somewhere in the final common pathway
motor
Central input to the final common pathway is ______ inhibition

Damage results in _________ of the involved muscle group
tonic

overactivity
Technologic Assessment: Lumbar Puncture
CSF evaluation indicated in specific circumstances

Urgent (do not wait for imaging):
Acute CNS ________ in the absence of focal neurologic signs

Less urgent (wait for brain imaging):
Vasculitis, SAH, increased intracranial pressure in absence of ________ on MRI or CT
infection

mass lesion
Lumbar puncture:

Also use for intrathecal therapy for fungal or carcinomatous ________

Symptomatic treatment for _________ from idiopathic intracranial hypertension or SAH
meningitis

headache
Lumbar Puncture:
What to look at in ____ (what to order) -
Cell count
Differential
Protein
Glucose
Bacterial cultures
Color and clarity ~ Cloudy CSF should be centrifuged and examined for ___________ in comparison with water
CSF

xanthochromia
Gram stain
Fungal viral and TB cultures
Cryptococcal and other antigens
Syphilis
Lime titres
Malignant cytology
PCR for specific viruses
Opening and closing pressures
LP special studies
Lumbar puncture: Contraindications

________ -
Tissue infection at puncture site

________ -
Known intracranial or spinal mass lesions
Increased intracranial pressure due to mass lesions
Coagulopathy due to thrombocytopenia, anticoagulation therapy, or bleeding disorders
Absolute

Relative
Transtentorial or foramen magnum herniation
Spinal epidural hematoma
Spinal abcess
Herniated or infected intervertebral disc
Meningitis
Reaction to local anesthesia
More common ~ Headache and backache
LP Complications
Helpful in situations where patients cannot be adequately examined or interviewed
They are:
Electroencephalography
Electromyography
Nerve conduction studies
Evoked potentials
Electrophysiologic studies
Electroencephalography:

Mostly used to investigate ________
Documents encephalopathy by documenting slowed background electrical activity in the brain
Also used in the evaluation of ________
seizures

brain death
Electromyography:
Used in the ddx of _______ disease, neuromuscular junction disease, peripheral nerve disease, and anterior horn cell disease

Nerve Conduction Studies:
Show decreased ________(axonal neuropathy)
Show decreased _______(diagnostic of demylenating disease).
muscle

amplitude

velocity
Nerve Conduction Studies:

Visual evoked potentials -
Used in the evaluation of ___
Asymmetrical slowing of the cortical response to a visual pattern stimulation suggests __________ of the optic nerve and optic visual pathways

Brain stem auditory evoked potentials -
Helpful in diagnosis of disease of CN ___ or its projections
Helpful to dx ______ in infants
MS

demyelination

VIII

deafness
Imaging:
MRI and CT are ______ in most neurologic diseases
Also, many abnormal findings on CT and MRI have no bearing on the neurologic problem responsible for the patient’s symptoms
*However, they provide important diagnostic precision for ________ lesions*
normal

central nervous system
Imaging:

_____ is used for most purposes
Provides more detail
Gets images in horizontal, coronal, and vertical planes simultaneously
Used for functional imaging and spectroscopy
Good for eval of congnitive and metabolic disorders, _______, and MS

____ has greater accessability, quicker to get, and tolerated better by the patient
Detects acute _________
Preferred for _________
MRI

epilepsy

CT

hemorrhages

emergencies
Imaging:

MRI and CT -
Both with __________ are useful in tumors, abcesses, and other processes that alter the blood brain barrier

____:
Allows noninvasive visualization of the major vessels of the head and neck
contrast media

MRA
Imaging:

Conventional _________ is used to evaluate intracranial vascular abnormalities
Small aneurysms, AVM’s, and inflammation of small blood vessels

Non invasive __________
Can define stenotic vessels and with transcranial Doppler can alow characterization of blood flow in intracranial arteries

Single photon emission CT helpful in eval of intracranial _______
angiography

ultrasonography

blood flow
PET (positron emission tomography):
Imaging tool that demonstrates _______ abnormalities
Useful for evaluating local abnormalities of ___________ & _________ metabolism
Expensive and limited to specialized centers
PET is useful in defining site of origin of focal ______
Also, may be used to differentiate Alzheimers Dz from other forms of ________, and to gain early dx of Alzheimer’s disease
metobolic

glucose and oxygen

seizures

dementia
Parkinson’s Disease and Huntington’s Disease
Movement Disorders
Signs and symptoms of motor system disease:

_____ disorder -
Difficulty with coordination, balance, and rapid movements
Normal muscle strength, no muscle wasting
Muscle tone increased, with spacticity or ridgidity

____ Disorder -
If weakness proximal: climbing or descending stairs, rising from chair, lifting heavy objects over head
If weakness distal: stumbling and tripping, problems fastening buttons, and opening locks or doors w/hands
CNS

PNS
Is a hypokinetic (not enough movement) disorder with akinetic/rigid syndrome (increased muscle tone throughout the range of motion)
Will not vary with passive ROM by the examiner
Cogwheel rigidity
Superimposition of tremor on underlying rigidity
Parkinson’s Disease (PD)
PD:
Occurs in all ethnic groups
Equal ____ distribution
Most common variety is _______
Begins mostly between ages ______
Affects up to 1 million people in the US
Leading cause of _______ in people over age 65
sex

idiopathic

45 and 65

neuro disease
4 diagnostic criteria for PD
Tremor
Bradykinesia
Postural instability
Muscle rigidity
PD Clinical findings/diagnosis:
Tremor, rigidity, bradykinesia, and postural instability are the cardinal features

Tremor -
4-6 cycles/sec
Noticed more at ____
Worsened by _____
Less severe during voluntary activity
Mostly confined to one ___ for years before it becomes generalized
rest

stress

limb
PD Clinical Findings/diagnosis:

Rigidity -
Increased _______ to passive movement
Characteristically ______ posture seen in many patients

Bradykinesia -
Most disabling symptom of PD
_______ in voluntary movements and reduction in involuntary movements such as swinging arms while walking
However, these voluntary movements may be temporarily regained during emergency
resistance

flexed

Slowness
PD Clinical Findings/diagnosis:

Other signs -
________ face with widened palpebral fissure
Infrequent blinking and fixed facial expression
________ of scalp and face
__________(flutter of closed eyelids)
Tremor about the mouth and face
_______ sign
Drooling
Soft, quiet voice
_________ (decrease in size of letters written in sentences or words)
Shuffling gait, loss of arm swing, difficulty in stopping, propensity to fall
Immobile

Seborrhea

Blepheroclonus

Myerson’s

Micrographia
PD Differential Diagnosis:
_____ (hypokensia and slight tremor)

________ (expressionless face, reduction in activity)
These two disorders co-exist so may be difficult to differentiate
May require trial of antidepressants to differentiate

______ disease -
Early age of onset
Keyser-Fleischer rings
Hepatitis

_________ disease -
Family history
Accompanying dementia
Old age

Depression

Wilson’s

Huntington’s
PD Treatment – drug treatment not required early in disease, but should be discussed w/patient

Medical Measures -
_________:
helpful if mild sx w/no disability
Improves all clinical features of Parkinsonism but MOA unclear

Side effects-
Restlessness, confusion, depression, skin rash, edema, nausea, constipation, anorexia, postural hypotension, cardiac arrythmias.
SE’s unusual with usual dose of ________
Amantadine

100 mg/BID
PD Treatment: Anticholinergic drugs (______)
Helpful in relieving tremors and rigidity
Started in small dose with increases in increments until benefits occur or side effects limit further increases

Side effects-
Dry mouth, nausea, constipation, palpitations, arrythmias, urinary retention, confusion, agitation, restless, drowsiness, mydriasis, increased IOP’s

Contraindications-
BPH, narrow angle glaucoma, obstructive gastrointestinal disease
Cogentin
PD TX: ________
converted to dopamine

SE- N/V, diarrhea, tarditive dyskinesia, facial ticks, choreathetoid movements

______ phenomenon: 4-6/day cycles
the drug will work for a matter of time then not anymore
thought to be due to falling plasma levels
Levodopa

on/off
PD TX: Levodopa/Carbidopa (_______)
Carbidopa prevents levodopa breakdown
When given together, amount of levadopa given for beneficial effects can be less
Result is fewer side effects, with exception of “off and on” phenomenon or dyskinesias
Sinemet started in small dosages of __________ and increased depending on response

Contraindications-
Psychotic illnesses
Narrow angle glaucoma
Concomitant MAOI usage
Use with care in _____, may worsen disorder
Sinemet

25mg carbidopa and 100mg levodopa TID

PUD
PD TX: ________ agonists (Permax and Parlodel)
Dopamine agonists which acts on dopamine receptors

SE-
Anorexia, nausea, vomiting, constipation, postural hypotension, digital vasospasm, dyskinesias, headache
Some reports of pericardial, plural, or pulmonary fibrosis
Pergolide and bromocriptine have been replaced by other agents because of theses side effects
Newer meds are ________ & ________ (Requip and Mirapex)
Lower incidence of dyskinesias and “off and on” phenomenon
Dopamine

pramipexole and ropinerole
PD TX: COMT inhibitors
Catecholamine–0–methyltransferase inhibitors reduce the metabolism of levodopa to methyldopa leading to longer plasma levels and more dopamenergic stimulation of the brain
________ & ________ currently available
Adjunct to levodopa in patients with response fluctuations or inadequate response who have failed other adjunctive therapies
Given _____ with Sinemet but Sinemet dosages may have to be reduced up to 1/3 to avoid dyskinesias
Tolcapone and entacopone

TID
PD TX: COMT Inhibitors
Side effects are diarrhea and rare cases of ____ with tolcapone
_____ should be ordered every 2 weeks for the 1st year of patients receiving tolcapone
Entacapone is the preferred agent because of no liver toxicity and no need for LFT’s
______ is the commercial preparation consisting of levodopa/carbidopa combined with entacapone
FHF

LFT’s

Stalevo
PD General Measures:

_______ & _______ therapy

Aids to daily living:
Rails
Banisters
Larged handle table utensils
Non slip table mats
Non slip surfaces in bathrooms
Voice amplification devices
Physical and Speech
PD Surgical measures:

Thalamotomy or pallidotomy for patients who are unresponsive to medical treatment or have intolerable side effects to meds
_________: surgical procedure to destroy the globus pallidus to relieve involuntary movements or muscular rigidity
___________: ablation of selected portion of the thalamus to relieve tremors
Pallidotomy

Thalamotomy
PD: ______________
High frequency electrical thalamic stimulation supresses the rest tremor of PD
Bilteral stimulation of the subthalamic nuclei or globus pallidus internus may benefit all the features of PD

Advantages -
Is reversible
Causes minimal or no damage to the brain
*Is the preferred surgical approach to treatment*
Deep Brain Stimulation
PD: Secondary Causes

__________ Parkinsons-
Mostly ________ medications
Provoke a bradykinetic/rigid syndrome

Examples:
Established as a cause~
Phenothiazines and butyrophenones
Metaclopramide (_______)
reserpine
Reported as a cause~
Lithium
Phenytoin
ACE inhibitors
Drug Induced

neuroleptic

Reglan
PD: Secondary causes

________ Disease-
Inclusion bodies found in vacuoles of injured neurons
3 types exist based on where they are found
When found only in brain stem there is no difference between Lewy body Dz and PD
Lewy Body
PD: Secondary Causes

_________ Parkinsonism-
Signs of PD
Microangiopathic changes in basal ganglia

______ Parkinsonism-
Carbon monoxide intoxication causing bilateral necrosis of the basal ganglia
Chronic esposure to _______
Parkinsonian sx after usage of street drug _____
Vascular

Toxic

manganese

MPTP
Huntington’s Disease:
Progressive autosomal dominant neurodegenerative disorder affecting motor function, cognition, and behavior
Characterized by _______ & ______
Occurs throughout the world in all ethnic groups
5 cases/100,000 population
Clinical onset between ______ years of age
_______ outcome within 15-20 years from onset
chorea and dementia

30 and 50

Fatal
Huntington’s Clinical findings:
Initial sx are abnormal movements or ________ changes
Earliest mental changes are _________-
Irritability
Moodiness
Antisocial behavior
Psychiatric disturbances
Eventual dementia
intellectual

behavioral
Huntington’s:
_________ initially fidgetiness or restlessness
Eventually choreiform movements and dystonic posturing
Progressive ________ and akenesia sometimes occurs with dementia
Dyskinesia

rigidity
Huntington’s Imaging:
________ demonstrates cerebral atrophy of caudate nucleus
____ shows reduced glucose utilization in an anatomically normal caudate nucleus
CT scan

PET
Huntington’s DDX:
________with no family hx of Huntingtons should not be attributed to Huntingtons

_________ causes of chorea:
Stroke
SLE
Paraneoplastic syndromes
Infection with HIV
Medications
In younger patients, after Strep infection-
Rare, called _________, self limiting
Chorea

Non genetic

Sydenham’s chorea
Huntington’s Treatment:
No cure, can’t halt progression, treatment is _________
Dopamine receptor blocking agents such as _________ or __________ may control dyskinesia or behavioral problems
_________ (antipsychotic) for behavioral disturbances
symptomatic

phenothiazines or haloperidol

Clozapine
_________ Syndrome
Motor Tics are involved in 80% of the cases
20% have phonic tics
Usually all patients develop combination of motor and phonic tics
Tourette’s
Tourette’s: Tics
1st noted in childhood between ages 2 and 15

_______ tics-
Face, head, and shoulders
Sniffing, blinking, frowning, shoulder shruging, head thrusting
Can be self mutilating (biting lips, tongue, pulling hair)

_______ tics-
Grunts, barks, hisses, throat clearing, cough
_________ – obsene speech utterances
_________ – repitition of speech of others
Motor

Phonic

Coprolalia

Echolalia
Tourette’s:
Chronic disorder with relapses and remissions
___________ behaviors which may be more disabling than tics
PE: normal except for ____
________ disturbances due to cosmetic and social embarassment
Obsessive-compulsive

TICS

Psychiatric
Tourette’s Treatment:
_________ is DOC
_________ (Klonopin) may be helpful and avoids the long term side effects of haloperidol
________ is a dopamine-blocking drug related to Haldol that may be helpful in patients who have not responded to Haldol
Haloperidol

Clonazepam

Pimozide
Cerebrovascular Disease: disorders of the arterial and venous circulatory system of the central nervous system

_________: Onset of abrupt sx due to inadequate blood flow (ischemic stroke) or hemorrhage into the brain tissue (parenchymal hemmorhage) or surrounding space (subarachnoid hemorrhage).
most frequent cause of morbidity in developed countries
Stroke
Types of stroke: Ischemic stroke

_________ stroke is thrombotic or embolic occlusion of major artery
_______ ischemia is from inadequate cortical profusion (after cardiac arrest or V-fib)
___________ (CO poisoning or asphyxiation) can cause stroke, but is rare
Focal ischemic

Global

Isolated cerebral hypoxia
Hypertension
Diabetes
Hyperlipidemia
Cigarette smoking
Cardiac disease
AIDS
Drug abuse
Heavy alcohol usage
Family history
Risk Factors for Stroke
Ischemic Strokes: ________ ischemia
can result from thrombotic or embolic occlusion of vessel that reduces blood flow to tissue
Also can be due to diminished systemic profusion
Prolonged ischemia results in infarction
Results in necrosis of neurons, glia, and endothelial cells
Cerebral
Ischemic Strokes: Global cerebral ischemia
from __________ or ______

Some neurons more sensitive to global ischemia -
Hippocampus (learning and memory)
Perkinje cells of cerebellum
Deeper layers of cerebral cortex

Pure hypoxia causes lethargy and confusion but rarely irreversible brain injury
Cardiac arrest or V fib
Ischemic Stroke: Etiology

______ abnormalities-
Atherosclerosis, vasculitis, vasospasm, compression (tumor), fibromuscular dysplasia (moyamoya dz), dissection

________-
Cardiogenic (atrial fib, mural thrombus, valvular vegetations, myxoma), fat, air, paradoxical, hypercoaguable state, homocystinuria, protein C or protein S deficiency
Mural

Embolism
Ischemic Stroke: Etiology

___________ accounts for 2/3 of strokes
Embolization of plaque to distal vessel
Insitu thrombus
Certain sites of cerebral vasculature are more prone to plaque development

____________ make up most of the remaining 1/3
A-fib, mural thrombus, myxoma, valvular vegetations
Athroschlerosis

Cardiogenic emboli
Cerebral Edema: Intercelluler (________) or interstitial (________)

Intercellular develops in ischemic neurons when __________ fail

Vasogenic occurs due to damage to __________ cells, disrupting BBB and allowing macromolecules (plasma proteins) to enter the interstitial space

Fluid accumulates over 3-5 days after ischemic stroke and can increase brain water content by 10% leading to transtentorial herniation and death
cytotoxic

vasogenic

ion channel pumps

endothelial
______: Transient neurologic defect due to reduced blood flow lasting less than 24 hours and followed by full functional recovery
Most resolve within 1 hour
Those that last longer should be worked up for alternative explanation
Complete stroke means infarction, in TIA there is no infarction
TIA
TIA:
Maximal clinical deficit in TIA occurs at onset of symptoms
Symptom progression in TIA is called __________
Factors contributing to this are-
Propagation of a ________
Progession of cerebral edema or hemorrhage to an _________
Hypotension, fever, hypoxemia, or hypoxia may also worsen the condition
Stroke in evolution

thrombus

infarction
Lacunar Stroke:
A cerebral lacunae is a small deep infarction involving the penetrating branch of a large cerebral artery
Associated with _________
In normotensive patients may be result of microathroma of penetrating arteries of basal ganglia or thalamus

Clinical syndrome:
Usually pure motor _________
Sometimes includes weakness and ataxia with hemiparesis known as _________
chronic hypertension

hemiparesis

Ataxic hemipareisis
Major Stroke Syndromes: Internal Carotid Artery
TIA’s in the anterior circulation affect the retinal artery or MCA

Retinal artery symptoms:
_________ vision in one eye or monocular blindness (__________)
Retinoscopy (fundoscopy) shows refractile arterial spots which are ________ crystals that have become detached from cholesterol plaque
Graying out

amaurosis fugax

cholesterol
Major Stroke Syndromes: Internal Carotid Artery

Most anterior circulation TIA’s are from significantly _______/_______ ICA
Others are caused by ____________
Others from spontaneous arterial _______
stenotic/ulcerated

cardiogenic embolism

dissection
Major Stroke Syndromes: Internal Carotid Artery

Arterial occlusion of ICA results in _________ hemiplegia and hemisensory loss of the MCA territory
_________ accompanies the occlusion and deficit depends on collateral circulation
Clinical recognition of ICA stenosis may be unreliable, because _______ doesn’t distinguish external carotid from ICA
contralateral

Headache

bruit
Major Stroke Syndromes: ___________ artery

Embolism causes most of these
Main MCA occlusion causes contralateral hemiplegia, hemianesthesia, and homonymous (lateral) hemianopsia with gaze away from the hemiplegic side
Middle Cerebral
Major Stroke Syndromes: Anterior cerebral artery

Occlusion of the ACA distal to the anterior communicating artery causes weakness and sensory loss in the contralateral ___
Other manifestations:
_______________
______ – akinetic mutism if bilateral (decrease in movement, speech, thought, and emotional reactions)
leg

Urinary incontinence

Abulia
Major Stroke Syndromes: ___________

Dizziness (vertigo), diploplia, ataxia, sensory and motor sx, drowsiness
Difficult to differentiate vertebrobasilar vertigo from labyrinthine but isolated positional vertigo is more likely to be labyrinthine
Vertebrobasilar ischemia
Major Stroke Syndromes: Occlusion of ______________

Occlusion of these arteries and/or their branches (PICA, AICA, and SCA) cause specific problems
Acute infarction of the cerebellum from occlusion of any of these causes -
Swelling in the posterior fossa
Obstruction of the 4th ventricle
Obstructive hydrocephalus
vertebral or basilar artery
Major Stroke Syndromes: Occlusion of vertebral or basilar artery

_______ artery occlusion produces massive brain stem dysfunction and is often fatal

If medulla is spared, the _______ syndrome can occur:
Quadriplegic
Can only communicate by means of ___________
Basal

locked in

vertical eye movements
Major Stroke Syndromes: ____________ occlusion

Contralateral hemiparesis
Hemisensory loss
Amnesia
Hemianopsia
Central vision spared due to collateral vessels from MCA
Posterior cerebral artery
Major Stroke Syndromes: Central Venous Thrombosis

Occlusion of the ______ sinus due to hyperviscosity or hyercoagulability
Common in _________

Clinical picture:
Papilledema, headache, or seizures
Diagnosis based on imaging showing hemorrhagic infarcts in parasagittal distribution
____ or ____ often shows the filling defect
sagittal

pregnancy

MRA or CT
Diagnosis of Stroke: Two questions

What is the ________?
Focal ischemic/thrombotic or embolic
Global ischemia/hypoprofusion
Hemorrhage

Where is the ______?
mechanism

lesion
Diagnosis of stroke: Physical Exam

Determines lesion _________
Identify clues to pathogenesis
_________ exam - BP, cardiac rhythm
Opthalmoscopy - _______ & _______ emboli
Information regarding severity and chronicity of HTN
_________ in cerebral venous thrombosis
localization

Cardiovascular

Platelet and cholesterol

Papilledema
Diagnosis of Stroke: Lab

_____
_____
Coag screen
_______ profile
_________ profile necessary in young person with venous sinus thrombosis
CBC

ESR

Lipid

Hypercoagulable
Diagnosis of Stroke

____ is most reliable test for differentiating ischemic stroke from hemorhage
Limitation is that only 5% of ischemic strokes are visible in 1st 12 hrs

____ is used to verify infarct if diagnosis remains in doubt

Anterior circulation best assessed with duplex ultrasound or ____
CT

MRI

MRA
DDX:
TIA’s vs __________ migraines
Some _______ are followed by hemiparesis
Acute onset of stroke differentiates it from other brain lesions
Strokes and seizures can co-exist
Generally, stroke rarely manifests with an alteration of _________
hemiplegic

seizures

conciousness
Treat HTN
Smoking cessation
Treatment of DM
Treatment of hyperlipidemia
Stroke Prevention
Stroke Prevention: TIA

Strong risk factor for stroke
5% risk per year
Antiplatelet therapy with ____, _________(ticlid), or _________(plavix) prevents secondary events
Hospital admission for new onset and recurrent TIA’s
Imaging studies should be performed and decision made for medical or surgical rx
ASA

ticlopidine

clopidogrel
Stroke Prevention: Carotid stenosis

Asymptomatic _______ or _______ of less than 60% can be treated with antiplatelet therapy
Bruit of more than 70% stenosis requires _________ to reduce stroke risk
60%-70% treatment decision made on case by case basis
bruit or stenosis

endarterectomy
Stroke Prevention:

Atrial Fib - Treat with _________ to INR of 2-3

Prosthetic Heart Valve - Long term ________

Bacterial endocarditis - Do not anticoagulate as risk of ___________ from septic embolism is high
coumadin

anticoag

cerebral hemorrhage
Stroke Management: General measures

Emphasis initially is to reduce the risk of complications from ________(pneumonia, DVT, UTI)
Early intervention by PT, OT, and speech therapy
Careful observation of ________ ability helps reduce mortality
Aggressive Rx of ____ & ____
Prevention and treatment of _________ may reduce extent of stroke
Awareness and treatment of post stroke ________ enhances rehab
immobility

swallowing

HTN and DM

hyperthermia

depression
Stroke Management: Anticoagulants

___________ therapy is treatment of choice to prevent recurrance
_________ is important in atrial fib, recent MI’s and thrombus propagation
_______ necessary before starting heparin to make sure there is no intracerebral or subarachnoid hemorrhage
Coag studies, platelet counts, and tests for hypercoag states before therapy starts
Uncontrolled HTN (SBP > 200 mm/hg) or active _____ is contraindication to anticoagulants
Antiplatelet

Anticoagulation

CRANIAL CT

PUD
Stroke management: Thrombolysis

Consider in patients who present within __ hrs of onset
IV __________
Risks and benefits must be explained to patient so decision be made rapidly
Risk is 6% for intracranial hemorrhage
Benefit is 50% chance of little or no disability at 6 mo with rt-tpa and 38% chance without it
Careful monitoring of BP and no ________ or ____ for 24 hours post rt-pa therapy
3

rt-pa (recombinant tissue-type plasminogen activator)

anticoagulants or ASA
Stroke Management: Cerebral edema

Only in large hemispheric infarct will cerebral edema be enough to cause _________
If herniation, intubation and hyerventilation cause transient ____________ to reduce intracranial pressure
_______ used also, but is transient in its effect
herniation

vasoconstriction

Mannitol
Management of Stroke: Stroke rehabilitation

The majority of deaths from stroke are from _______ complications rather than neuro complications
Pneumonia
Sepsis
MI
DVT
_______ optomizes recovery and decreases medical complications
medical

Rehab
Intracerebral Hemorrhage:
May be diffuse (SAH) or focal intraparenchymal
Accounts for 20% of all strokes

Causes of spontaneous ICH -
__________:
HTN, Amyloid aniopathy, AVM’s, drugs (amphetamines, cocaine, anticoagulants, thrombolytics) and tumors
______:
Congenital aneurysms (85%), mycotic aneurysm, AVM’s
Intraparenchymal

SAH
Intracerebral Hemorrhages: Hypertensive ICH

Occur at same sites affected in ______ infarcts
Clinical findings help localize the site
_________ severity correlates with size
Diminished ________
________ - More prominent in acute phase of ICH than in ischemic stroke
lacunar

Headache

alertness

Seizures
Intracerebral hemorrhages: Lobar hemorrhage

Mostly in ________ distribution unlike hypertensive hemorrhage
Smaller than hypertensive ICH’s
More ______ prognosis

Causes
_________: AVM’s or sympathomimetic drug ingestion
________: congophilic amyloid angiopathy
Signs tend to develop more slowly
peripheral

benign

Young persons

Elderly
Intracerebral hemorrhage: Diagnosis, management, and prognosis

____ is test of choice (MRI less sensitive in early stage)

Management: depends on size and location
Acutely the mass effect is much greater than in an infarct, with greater risk of ___________
Chronically prognosis is better in __________ than ischemic stroke
CT

herniation and death

hemorrhagic
Intracerebral hemorrhage: Treatment

Directed at reducing ________
By medical decompression with __________ or ________
By ________ decompression (rarely) - Urgently in cases of cerebellar hemorrhage where patient at risk for sudden deterioration from obstructive hydrocephalus or from direct pressure on brain stem
mass effect

hyperventilation or mannitol

surgical
Intracranial anneurysms: Three types

________ - Eratic dilations of large arteries
Usually basilar or intracranial carotid
Rarely rupture but compress structures causeing local neurological dysfunction
Not usually accessible for surgical repair

______ - In bacterial endocarditis where septic emboli lodge in vessels
Multiple and in distal arterial tree
Can be repaired surgically if no response to antibiotic therapy
Fusiform

Mycotic
Intracranial anneurysms: Three types

______ - Berry aneurysms
Form at arterial bifurcations
80% located in anterior circulation
Arise from congenital defect in the arterial media and elastic lamina and from gradual deterioration due to hemodynamic stress
Higher incidences in ________ disease patients and in _______ syndrome
6% of population have saccular aneurysms
Incidence of rupture only 10/100,000 pts
33% of those die before hospital, 20% in the hospital
30% recover without disability
Saccular

polycystic kidney dz

Marfan’s
________: a chronic condition of seizures with sudden and usually unprovoked attacks of subjective experiential phenomena, altered conciousness, or involuntary movements
Epilepsy
_______- are from abnormal brain electrical activity and are a common sign of brain dysfunction

Can occur during the course of many medical or neurologic illnesses where brain function is temporarily deranged (symptomatic seizures)
Self limited and do not persist if underlying disease corrected
Can occur as reaction of brain to physiologic stress
Seizures
Those with limited part of the cerebral hemisphere involved are _______ or _______ seizures

Diffuse cerebral cortex involvement seen in _________ seizures

Seizures are dynamic and may evolve:
Simple partial into _______
Partial into _______________
partial or focal

generalized

complex partial

secondary generalized clonic tonic seizures
__________ seizures occur when epileptic electrical discharge remains limited to a focal area of the cortex
Normally patients can interact with environment
Limitations imposed on specific brain functions only
May be sensory and/or psychological phenomena
60% have auras
Location of focus is important for diagnosis and helps direct diagnostic testing
Simple partial
Simple partial seizures:
Can also occur with _____ signs
Clonic (jerking) tonic (stiffening) movements of a body part
Face and hand often involved due to large cortical representation
Clonic movements progress in orderly sequence (“__________”) that reflects homunculus representation

produce contralateral flexion and elevaton of the arm with turning of the head and eyes and tonic extension of the ipsilateral arm (“_________”)
Other signs include speech arrest, vocalization, and eye blinking
motor

Jacksonian march

fencer’s posture
Simple partial seizures:
May be followed by __________ state of the involved area

_______ may follow simple partial motor seizure
Numbness, a sensory seizure
_______, and occipital lobe seizure
post ictal depressive

Weakness

Blindness
________________:
Impair consiousness and produce unresponsiveness
Or, altered conciousness and automatisms such as lip smacking, chewing, swallowing, other erratic behavior
Preceded by _____(de ja vu, visual)
Complex Partial Seizure

aura
____________:
Begin diffusely and involve both cerebral hemispheres simultaneously
Subdivided according to presence and character of motor manifestations during the seizure
Generalized seizures
Generalized seizures: _____________
Abrupt LOC with tonic extension of trunk and limbs (tonic phase)
Accompnied by epileptic cry which is air forced across contracted vocal cords
This is followed by the clonic phase
Symmetric bilateral muscle jerking
Some patients will have only a tonic or clonic phase
Generalized tonic/clonic seizures (grand mal)
Generalized seizures: Tonic/clonic

Generally there is __________, but fecal incontinence is rare
Seizure lasts about 90 seconds usually, followed by post ictal phase
Post ictal phase: 15-30 minutes of __________ state
Followed by headache, muscle soreness, mental dullness, lack of energy and mood changes lasting up to __ hours
urinary incontinence

lethargic confused

24
Transient physiologic changes of Clonic/Tonic seizures:
Blood _______
Lactic acidosis
Elevated __________ levels
Increased levels of _________, prolactin, corticotropin, cortisol, and growth hormone
hypoxia

catecholamine

creatine kinase (CK)
Compications of C/T seizures:
_____ trauma
________ compression fractures
Shoulder dislocation
Aspiration pneumonia
________ - Acute pulmonary edema, cardiac arrythmias, suffocation
Oral

Vertebral

Sudden death
Generalized Seizures: _____________
Mostly in children
Sudden momentary lapses in awareness
Staring with rhythmic blinking
Occasionally small clonic jerks of hands or arms
Last 10 seconds with no post ictal period
Behavior and awareness returns to normal immediately
Absence seizures (petit mal seizures)
Generalized seizures: ____________
Rapid recurring brief muscle jerks
Bilateral or unilateral
Ranges from small movements of face and hands to massive spasms of head, limbs, and trunk
Repeated myoclonic seizures may build to general clonic-tonic seizures
Occur in clusters after waking, or when falling asleep
Myoclonic seizures
Febrile seizures:
The most common cause of convulsion (seizure) in children is _______

Epidemiology:
Affects 3-5% of all children under age 5
Occurs between ages 6 mo and 4 yrs
Can occur in kids up to 7 years
30% have more than one attack
Recurrence greatest if seizure occurs before age __ or there is family hx of febrile seizures
FEVER

1
Febrile seizures:
Usually no long term consequences
But, may increase the risk of developing ________ later
Low in most children (2-3%)
Higher (10-13%) in those who-
Have _______ or focal seizures
Have a family history of afebrile seizures
Are neurologically _______ before the 1st febrile seizure
epilepsy

prolonged

abnormal
Febrile seizures _____ cause:
Mental retardation
Poor school performance
Behavior problems
do not
Benign partial epilepsy of childhood with Central-Midtemporal Spikes:

One of the most common epileptic syndromes in childhood
15% of all peds epilepsies
Begin between ages 4 and 13
Occur mostly at _______
Parents see only _________ activity
Focal episode is usually missed
night

tonic-clonic
Benign partial epilepsy of childhood with Central-Midtemporal Spikes:


When occurring during day-
Focal episodes are one sided facial twitch, ______ arrest, drooling, ________ of the face, teeth, gums tongue and inner cheek
May be very minor and go unnoticed
May progress to hemi clonic-tonic activity

____ distinctive for eliptiform discharges over the central and mid-temporal regions
Prognosis-
Good, with resolution by mid to late adolescents
Treated with __________(Tegretol) which prevents further attacks
speech

paresthesias

EEG

carbamazepine
__________________:
Most common epileptic syndrome in adults (40% of epileptic cases)
Begins in late childhood or adolescence
Mostly complex partial, some which generalize
Arises typically from medial temporal limbic structures but can be from cavernous malformations, cortical dysplasia, glial tumors and *scars from previous _________ or __________*
Temporal Lobe Epilepsy

head injuries or encephalitis
______________:
Chances relate to severity of injury
Severe head injury defined as
Cerebral contusion
Intracerebral or intracranial hematoma
Unconcciousness or amnesia lasting more than 24 hours
Persistant abnormalities on neuro exam
Post traumatic epilepsy
Post traumatic seizures:
Majority develop seizures within ____ years of injury
But new onset seizures can occur up to 5 yrs later
2/3 of patients have partial or secondarily generalized seizures
No increased risk with _____ head injuries such as contusion or hematoma
1-2

mild
Diagnosis of Epilepsy:

________ is the most important diagnostic test for epilepsy
Useful in:
Diagnosis
Classification of seizures
Identifying epileptic syndromes
Making therapeutic decisions
EEG (electroencephalogram)
Seizure DX: EEG

With clinical findings EEG patterns showing ______ or _______ are support the diagnosis of epilepsy
Focal epileptiform discharges in __________
Generalized epileptiform discharges in __________-
No interictal abnormalities on EEG’s can prove or disprove epilepsy
Can only establish diagnosis by EEG tracing during a clinical attack (hard to do)
Also 2% of normal people may have _______ EEG’s
In children, this may be a marker of a genetic trait
spikes or sharp waves

focal epilepsy

generalized epilepsy

abnormal
Diagnosis: EEG

40% of epileptic pts may show epileptical waveforms on _______
Chance of this is enhanced by ___________ 24 hours before test
Pt sleeps during some of the EEG recording
______ EEG’s increase yield of positive tracing
initial EEG

sleep deprivation

Serial
Diagnosis: Imaging

____ identifies structural brain pathology that may be associated with seizures (in concert with EEG)
Should get MRI on all patients over ___
Also, MRI in all children with-
_______ seizures
Abnormal neuro findings
Focal _______ wave abnormalities on EEG
MRI

18

partial

slow
Diagnosis: PET and SPECT (single proton emission computed tomography)
70% of patients with temporal lobe epilepsy have focal __________ areas on interictal PET scans that correspond to the epileptogenic focus
Abnormalities on PET and SPECT often seen even when ____ is normal
hypermetabolic

MRI
Diagnosis: Other tests

________, _________, & ______ are useful baseline before meds started
__________ screens in young adults with new onset seizures (blood and urine screens)
____ if suspicion of meningitis or encephalitis
____ in any young person with 1st generlized seizure if there is fam hx of arrythmia, unexplained death, or episodic unconciousness
Also, EKG in any patient with ________ or valvular dz
Electrolytes, LFT’s, and CBC

Substance abuse

LP

EKG

arrythmia
movement disorders
migraine
syncope
panic disorder
hyperventilation
TIA
alcoholic blackout
hypoglycemia
Seizure DDX
Treatment:
If cause of _________ seizures is corrected, anti-seizure drugs are not needed
Also not necessary in adults with _________ seizure with normal lab and clinical findings
symptomatic

single unprovoked
Treatment:
But, patients with focal neuro findings clinically, radiologically, or on EEG will probably have more seizures and may need ______
Also, social considerations may dictate treatment in patients with only one seizure
Generally, otherwise normal patients who will probably be non compliant do not need rx
_______ seizures should be treated to stop attacks completely
meds

Recurrent
The type of seizure should be defined and the preferred medication should be given in usual doses and then ________ until seizure control is complete or side effects occur
Seizures that are _______ require slow changes in medication doses
If seizures persist at toxic levels, or if major side effects occur, select another agent.
Do not stop one agent until another has been added
Otherwise, ___________ may result.
If seizures persist after two agents have been given to toxic levels, consider referral to a specialized center for complex combination therapy and seizure monitoring.
Toxic levels of some antiepileptics (particularly phenytoin and carbamazepine) can cause _______
increased

infrequent

status epilepticus

seizures
TX of __________:

Carbamazepine
Phenytoin
Valproate
Gabapentin
Lamotrigine
Topiramate
Simple & Complex partial
TX of __________:

Carbamazepine
Phenytoin
Valproate
Gabapentin
Lamotrigine
Topiramate
Secondarily generalized
TX of __________:

Valproate
Carbamazepine
Phenytoin
Lamotrigine
Tonic-Clonic
TX of __________:

Ethosuximide
Valproate
Lamotrigine
Absence
TX of __________:

Valproate
Clonazepam
Myoclonic & Tonic
Treatment: Surgery

____________: when seizures cannot be controlled by trials of two appropriate single agents or the combination of two agents
Medically intractable
Special Concerns: ___________
Major generalized motor seizures that follow so rapidly that a new one starts before the patient has recovered from the previous one
Can cause permanent _______
Most frequent cause is abrupt ________ from anti-seizure med in known epileptic
Other causes:
Withdrawal from ____ or other habitual drugs, cerebral infection, trauma, neoplasm, or hemorrhage
Status epilepticus requires urgent Rx and cause needs to be identified as soon as seizures controlled
Status epilepticus

brain damage

withdrawal

ETOH
Special concerns: Status Epilepticus

____________: lasts for hours to days.
May be highly focal or involve most of the limb or half the body
Causes:
Strokes, trauma, neoplasms, encephalitis
Severe _________ can produce partial motor and complex partial status epilepticus with complete resolution after hyperglycemia corrected
Partial motor status

hyperglycemia
Special Concerns: Status Epilepticus

__________: Sustained state of confusion
Schizophreniform or other bizarre activity
Some may be in stuporous state
Lasts for hours to days
Patients may resist assistance
Partial Complex status
Special concerns: Status Epilepticus

_________: two types
1. the more common one resembles partial complex status mostly in adolescence or young adults with petit mal history. Lasts less than 30minutes
2. Other type with automatisms and confusion lasts days to weeks

Most of these attacks can be halted with IV ________
Absence status

diazepam
Special Concerns: Psychosocial problems

Incompletely controlled epilepsy creates ________ problems for pts
Disorders that cause partial complex seizures are associated with aberrant __________
Frustration, depression, and suicide more frequent among epileptic pts
These problems helped most by bringing problem under complete control and encouraging pts to lead normal life
emotional

personality traits
Special Concerns:

Body contact sports avoided unless seizure free for _____
High risk sports to be avoided - High diving, high alpine cimbing, deep water swimming, underwater swimming, boxing
__________ restricted unless patient seizure free for specified time period
Epilepsy Foundation of America assists patients in social-vocational arenas
1 year

Drivers license
Discontinuing Meds:

Successful drug withdrawal more successful if initial control successful using _________ and EEG and neuro exam normal just prior to stopping meds
Seizure free intervals of _____ decrease likelihood of relapse
monotherapy

4 years
________: progressive loss of intellectual function with memory loss as the central feature

produce specific congition deficits:
Language, spatial processing, _____(learned motor behavior) and ___________(ability to plan and sequence events)
Dementia

praxis

executive function
Two divisions of Dementia:

______ dementia: cerebral cortex affected, causing problems with memory and language. Patients typically show severe memory impairment and aphasia
Alzheimer’s

________ dementia: dysfunction of brain beneath the cortex. Mostly changes in personality and attention span with slowed thinking.
Huntington’s, and AIDS related dementia
Cortical

Sub cortical
Neurodegenerative dementia:

Most common underlying cause of dementia-
________ disease
Frontotemporal dementia
Diffuse ________ disease
Alzheimer’s

Lewy body
Most dementia is __________

Potentially correctable causes are less than 10% of all cases:
Infection, metabolic, and nutritional diseases must be ruled out
All patients should have _________; liver, renal, and thyroid functions; vit ___ levels; and serologic tests for ______
Chronic infection and normal pressure __________ must be ruled out
___ should be performed on all patients with focal neuro signs and in those patients under 65 at onset of dementia
untreatable

electrolytes

B12

syphilis

hydro cephalus

MRI
Causes of potentially reversible _________ impairment include:
Drug effect
Depression
Thyroid disease
Vit B12 deficiency
hypercalcemia
Subdural hematoma
HIV
Normal pressure hydrocephalus
cognitive
___________ testing:
Characterizes the pattern of cognitive and memory loss and helps in DDx

_______ exam is bedside or office screening tool that identifies dementia patients
Emphasizes ________ & ________, so better for cortical than sub cortical dementia
Neuropsychological

MMS (mini mental state)

memory and language
Neuropshchological testing:

Also there are tests for
_______
“Show how you would comb hair”
“show how you would blow out a match”

________ processing
Clock drawing

_________(planning and sequencing)
Draw set of numbers on page and have the patient connect them in alphabetical-numerical order
Praxis

Visual spatial

Executive function
70% of all cases of dementia in the elderly

Incidence increases with age
Up to 30% of people over 85 years of age have ___________
ALZHEIMER’S DISEASE
AD Pathology:
Progressive loss of ________ neurons
Formation of ________(Aß/beta amyoid) in intraneuronal neurofibrillary tangles
Neurofibrillary tangles are twisted masses of protein fibers within nerve cells of the cerebral cortex of AD patients
cortical

amyloid plaques
AD: Etiology

Process starts in _________ and spreads to diffuse areas of cortex in the temporal, parietal, and frontal lobes
Deficiency of cortical _________ from the loss of neurons in the nucleus basalis is the basis for treatment with centrally acting acetylcholinesterase inhibitors
hippocampus

acetylcholine
AD: Pathogenesis - Two forms

Young onset or ______ form which is rare
3 specific genetic abnormalities are found in this form

More common is _______ form that occurs in patients over age 65
familial

sporatic
AD: Pathogenesis

Autosomal dominant AD (early onset form) like sx seen in pateints with ______ syndrome (Phil 21 trisomy) who are more than 30 years old
Suggests that chromosome 21 may harbor a gene responsible for AD
Aß is a cleavage product of the amyloid precursor protein, the gene for which is on chromosome 21
This may be important in the pathogenesis of AD
Also, apolipoprotein E gene was found to be a suceptability locus for sporadic AD in late onset AD
Down’s
AD: Clinical features

Early problems in ________
Impaired ________ abilities (lost in familiar surroundings; unable to copy geometric designs on paper)
But _______ retained despite advanced cognitive problems
Personality changes and behavioral difficulties
Wandering, inapproprite sexual behavior, and agitation
memory

visuospatial

social graces
AD: Clinical Features

End stage disease characterized by-
Near _______
Inability to sit up, hold head up, or track objects with eyes
Dfficulty with _______ and swallowing
Weight loss, bowel or bladder incontinence, and recurrent respiratory and urinary _________
mutism

eating

infections
AD: Treatment

Acetylcholinesterase inhibitors such as donepezil (________), rivastigmine (_______) and tacrine (______) should be considered
They produce modest improvement in cognitive function
May also help in ________ & _________ dementia
Aircept

Excelon

Cognex

vascular and Lewy-body
Diffuse Lewy-body disease:
These patients have clinical _________(slow gait, rigidity, balance problems) and prominent dementia
Lewy bodies are pathologic inclusions found in the brain stem, limbic system, and cortex
In Parkinson’s disease they are restricted to the ________ only
Parkinsonisms

brain stem
Diffuse Lewy-body disease:

Clinically, visual _________ and cognitive fluctuations are common
These pateints demonstrate a marked hypersensitivity to _______ therapy
Attempts to treat hallucinations may worsen the __________ symptoms
May be the 2nd most common cause of dementia after _________
hallucinations

neuroleptic

extrapyramidal

AD
Vascular Dementia (Multi Infarct dementia):

10-20% of elderly dementia pts have findings of focal ______ on MRI or CT with focal signs on PE
When dementia begins with stroke, and illness progression is ________, dx of vascular dementia is likely
strokes

stepwise
Vascular Dementia (multi infarct dementia):

Clinically-
Early __________
Flattening of ______
______ disturbances

TX is TX of risk factors:
________ control
_______ cessation
Diet modification
__________ (especially in selective settings such as atrial fib)
incontinence

affect

Gait

Blood pressure

Smoking

Anticoagulation
Frontotemporal Dementias:

Unlike AD, begins with marked _________ disturbances
______ dz is the classic form and is associated with ____
Patients are frequently socially disinhibited with personality change and compulsive behaviors (peculiar eating habits or hyperorality)
In contrast to AD, ________ function is preserved
behavioral

Pick’s

ALS

visuospatial
Parkinsons Disease:

50 % have _______ by the time they reach 85 (not AD)
Effects _________ more so than language or visuospatial processing
Thought processes slow down
Occurs relatively late in the disease
Many patients are taking drugs for PD that can induce ______, so always reduce dosages before diagnosing underlying dementia in PD patients
dementia

executive function

psychosis
___________ Disease:

A subacute dementing transmissible illness
Onset age 40-75 years of age
Incidence 1 in 1,000,000 population
4 forms
________(80-85%), familial (15%), iatrogenic (1%) and variant
Pathology: spongiform degeneration in widespread areas of the cortex
Incubation: years!!!
Creutzfeldt-Jakob

Sporadic
CJD:

Variants distinguished by -
Predominance of cerebellar sx
__________ hyperkenesias
Visual ______

90% of CJD patients have ________ fasiculations
All forms have relentless progression of _______ and personality changes over weeks to months
Extrapyramidal

agnosia

myoclonic

dementia
CJD:

Transmittable agent is a _____ protein, invulnerable to routine modes of antisepsis
____ can be tested for 14-3-3 protein, but is not 100% sensitive or specific for CJD
Risk factors greatest in _________ & ________

Prevention-
Avoidance of contaminated infected _______ tissue, electrodes, and neurosurgical tools
Also, can be contaminated by ________ transplants or contaminated cadaveric growth hormone from infected donors
No specific treatment
prion

CSF

butchers and medical office staff

brain

corneal
HIV:

HIV gets into CNS through monocytes and microglial system
Causes associated nuronal loss, vacuolization, and lymphocyte infiltration
Dementia characterized by __________ & ___________
Patients have executive dysfunction, impaired memory, poor ________, and apathy
Treatment of HIV (antivirals and reverse transcriptase inhibitors) may slow the progression of dementia
bradyphrenia and bradykinesia

concentration
Infectious agents:

Some infectious agents can cause chronic _________

They can cause subacute or chronic subcortical _________
meningitides

dementia
Normal-Pressure Hydrocephalus:

Triad of _______(subcortical), _____ instability, and urinary ________

Patients walk with “_____________”
Do not lift knees
Broad base
dementia

gait

incontinence

feet stuck to floor
Normal-Pressure Hydrocephalus:

Symptoms evolve over weeks to months
Imaging reveals __________ enlargement out of proportion to cortical ________ in the presence of dementia
MRI flow studies
Radionucleotide cisternography

Most important test is _____ removing large amounts of CSF followed by examination of patients gait and cognitive function
Removal of 30-40 ml of CSF
Should respond with improved _________ & ________ within minutes to hours
ventricular

atrophy

LP

gait and alertness
Normal-Pressure Hydrocephalus:

Pathogenesis -
Derangement of the _____ hemodynamics

Etiology and Treatment -
Potentially reversible dementia
_______ placement effective if normal-pressure hydrocephalus occurs following severe head trauma or SAH
Can also follow ____________ or be associated with CNS _____
CSF

Shunt

meningoencephalitis

tumor
Infectious Diseases of the Nervous System:

Localized to the CNS as ___________ or _______________ infections
Also, CNS manifestation of infections in the rest of the body
_______ disease
abscesses or parameningeal

Prion
Brain Abcess: Signs and sx of other space occupying lesions but with more rapid progression

Originate from extracerebral locations:
________ from unknown areas, lungs, or heart
__________ (parameningeal sites): otitis, cranial osteomyelitis, sinusitis
Sites of ________(recent or remote) or neurosurgical procedures
Infections associated with ___________________
Blood-borne

Direct extension

head trauma

cyanotic conginital heart dz
Brain Abcess: Pathogens

Mostly aerobic and anerobic _________
gram negative _______ (bacteroides and Prevotella)
Infection often polymicrobial
Culture is negative in 30% of antibiotic treated patients and 5% of those operated on prior to AB’s
Streptococci

anerobes
Brain Abcess: Diagnosis/presentation

May have no signs of systemic infection
½ with no fever or leukocytosis
Neck stiffness rare

Most common presenting sx:
_______ of recent onset (most common)
Followed by (if untreated)-
Increased severity
Focal signs such as __________ or __________
Followed by coma/obtundation

also after _______ surgery
Headache

hemiparesis or aphasia

oral
Brain Abcess: SX

May take hours, or days to weeks
_______ occur with abscesses involving cortical grey matter
_____ is non diagnostic and shouldn’t be performed. Can be normal/may aggravate transtentorial herniation due to rapid expansion of the abscess
Contrast ____ or ____ for diagnosis and monitoring
Seizures

CSF

CT or MRI
Brain Abcess: Treatment

Antibiotics or antibiotics with _______ or excision
_______ if mass effect or if abcess against ventricular surface (rupture into the ventricular system)
Surgery in posterior fossa lesion (brain stem compression potential)
Antibiotics alone if -
Surgically inaccessible
_______ abcesses
Early cerebritis stage
aspiration

Surgery

Multiple
Brain Abcess: Treatment

_________ plus _________ IV
If MRSA suspected (post op infection or IV drug usage) use _______
Follow resolution with CT or MRI
If med therapy only, continue AB’s for ___ weeks
Cephtriaxone

metronidazole

Vancomycin

8
Subdural empyema

Infection in space separating the dura and arachnoid
From direct extension of infected ___________ or less commonly untreated _________
Cortical venous _______ or _________ develops in about ¼ of cases
paranasal sinuses

chronic otitis

thrombosis or brain abscess
Subdural Empyema:

Sx initially those of chronic otitis or sinusitis
*_________ is universal feature*
______ and obtundation then ensue, followed by progressive mass and brain swelling leading to venous thrombosis or death from herniation

DDx is __________ -
Nuchal rigidity and obtundation in both
But, papilledema and lateralizing defects more common in sub dural empyema
Lateralized headache

Fever

meningitis
Subdural empyema:

Diagnosis - Contrast ____ & _____ can be diagnostic for empyema

Treatment -
prompt _________
high dose IV antibiotics
CT and MRI

surgical drainage
Malignant Otitis Externa:

Mostly in elderly patients with *________*
Etiology is ________

Presentation -
Rapid progression of _________
Ear pain, facial swelling
_________ of the skull base
Puralent meningitis with multiple _______
diabetes

pseudomonas

Ext Otitis

Osteomyelitis

CN palsies
Malignant ext otitis:

Treatment is urgent
______________ or 3rd generation ________
Surgical debridement (with above)

Mortality rate is high
Antipseudomonal penicillin

cephalosporin
Spinal Epidural Abscess:

Infection of epidural space about the spinal cord
Can cause _______ & ________, but usually responds to treatment

Frequency -
.05/10,000 hospital admissions in US
Higher in _______
death and paralysis

IV drug users
Spinal Epidural Abscess:

Present with acute or subacute _______
Usually _______(100.4 – 102.2)
Focal _____________ of spine
Stiff neck and headache

Pain may be mistaken for -
Sciatica
Visceral abdominal process
Chest wall pain
Cervical disc disease
If the condition goes unrecognized here, rapid weakness/paralysis can occur distal to the infection
At this point, spinal abcess should be assumed and neuroradiologic dx confirmed and tx started
back pain

febrile

percussion tenderness
Spinal epidural Abscess:

Pathogenesis -
________ sites most common source for hematogenous spread, especially in _________

Bacteriology -
Gram stain or culture from pus
Usually is ________
___ abcesses account for 25% in high risk pop.
Cutaneous

IV drug users

Staph Aureus

TB
Spinal Epidural Abcess: Treatment

Penicillenase-resistant penicillen empirically for staph (_______,_______)
_________ if MRSA suspected
With above, additional gram neg coverage with __________ or _________
Surgical decompression less necessary today due to early dx by MRI
Is necessary if neurologic complications occur
Dicloxacillin, Nafcillin

Vancomycin

3rd generation Ceph or quinolone
Cavernous Sinus:

A cavernous sinus thrombosis causes the cavernous sinus syndrome which is characterized by ______ of the eyelids and conjucntivae (______) of the eyes and _______ of the CN’s which course through the sinus
edema

chemosis

paralysis
Septic Cavernous Sinus Thrombosis:

Intracranial complication of _________
Most common organism is ________

Diagnosis:
Sinus imaging with attention to _________ & ________ sinuses
_____ shows absent “flow void” within a vascular structure
sinusitis

Staph aureus

ethmoid and sphenoid

MRI
Septic cavernous sinus thrombosis: Treatment

Early diagnosis with prompt ________ of the infected paranasal sinus
Specific antistaphylococcal agents such as _______ or _______ given IV
drainage

nafcillen or oxacillen
Myelin: Myelin is white and gives the name to the “_______” of the brain
white matter
__________: The process by which myelin of the central and peripheral nervous system is damaged or injured

Diseases of the CNS myelin are either acquired or hereditary

MS is the most common _______ disease of myelin
Demyelination

acquired
MS: Etiology

Involves autoimmune-mediated inflammatory _________ and axonal injury

Earliest event in MS lesion is breakdown of _____

MS also injures CNS neuronal axons which accounts for brain _______ and permanent damage as the disease progresses
demyelination

BBB

atrophy
MS: Clinical findings
Highest incidence in ________

Initially -
Weakness, numbness, tingling, or unsteadiness in a _____
Spastic paresis
Retrobulbar neuritis
Diploplia
Disequalibrium
Urinary _______ or ________ due to sphincter disturbance
Symptoms may disappear after a few days but on exam, a residual _______ may be noted
young adults

limb

urgency or hesitancy

deficit
MS: Clinical Findings (3 forms of dz)

___________(most common) -
Months or years after initial episode before new sx develop or original sx recur

Then relapses and remissions lead to disability
Weakness, spaciticity, and ataxia of limbs with impaired vision and urinary incontinence

Findings at this stage include -
Optic atrophy; nystagmus; dysarthria; sensory, cerebellar, and pyramidal deficits in some or all of the limbs
Relapsing remitting disease
MS: Clinical Findings (3 forms of dz)

__________________ -
In patients with relapsing remitting dz the clinical course changes to a steady deterioration rather than relapses

________________ -
Less common
Symptoms are steadily progressive from outset
Disability develops at an early stage
Secondary progressive disease

Primary progressive disease
MS: Clinical findings

Diagnosis made only when clinical picture indicates involvement of different parts of the ____ at different times
_________ & _________ likely to precipitate relapses
Relapses likely ____ months after due to increased demands and stresses of post partum period
CNS

Infection and trauma

2-3
MS: Imaging

____ most helpful by demonstrating multiplicity of lesions
When myelopathy alone presents with no clinical evidence of widespread disease, myelogram or MRI needed to r/o congenital or acquired surgically treatable lesion
MRI
MS: Lab and other studies

__________ response -
Evoked by monocular visual stimulation, by monaural click stimulation, and by electrical stimulation of a sensory or mixed peripheral nerve, is used to detect subclinical involvement of:
Visual pathways
Brainstem auditory pathways
Somatosensory pathways
Electrocerebral
MS: Lab and other studies

CSF may show ________ and elevated ______ concentration after an acute relapse
Elevated ____ in CSF present in many patients
lymphocytosis

protein

IgG
MS: Diagnosis

Should not be diagnosed unless there are ____ or more regions of the central white matter affected at different times
Diagnosis depends on above along with clinically relapsing remitting course of the disease
Or in patients with multifocal white matter dz but only one clinical attack
Or two attacks but only one white matter lesion
two
MS: Treatment

Recovery of acute relapses treated with ___________
High dose _____ mg/day for 7d followed by tapered dose for __ weeks
Preceded by __________ 1g IV for 3 days
corticosteroids

60-80 mg/day for 7 d

3

methylprednisone
MS: Treatment

In relapsing remitting or secondary progressive, ________ sub Q daily reduces exacerbation frequency
_________ therapy may help arrest the course of secondary progressive MS
Treatment for spasticity and neurogenic bladder needed in advanced cases
Patients must _____ during periods of acute relapse and excessive fatigue must be avoided at all time
beta interferon

Immunosuppressive

rest
_____________: disorders of the motor unit and of the sensory and autonomic peripheral nerves
Neuromuscular Diseases
Signs and SX of ________ disease:
Muscle weakness, wasting, fatigue, cramps, fasiculation, pain, stiffness

Signs and sx of _________ disease:
Decreased sensation (hypoesthesia,hypoalgesia), abnormal sensation (paresthesia), or painful sensations (dysesthesia)
motor neuron

peripheral nerve
Most sx of neuromuscular dz are _________ whereas focal CNS disease is usually __________

Most common acquired motor neuron disease is __________
symmetrical

asymmetrical

amyotrophic lateral sclerosis
Neuromuscular Diseases: Diagnostic Tests (Labs)

_____
_____
_____
_____
CK
LDH
AST
ALT
___________: Measurement of electrical activity arising from muscle fibers

Spontaneous activity in a single muscle fiber is called _________
Spontaneous activity of part of all or a motor unit is _________
Electromyography

fibrillation

fasiculation
Dz of the Motor Neuron:

If lower motor neuron only is involved the term ___________ is used

Progressive ________ motor neuron disorders that begin in utero, infancy, childhood, or adulthood
spinal muscular atrophy (SMA)

inherited
Bulbospinal muscular atrophy:

Disorder that alters the function of bulbar and spinal motor neurons (bulbar cerebellum, medulla, and pons)
Mean onset age ____ years
X-linked
_______, ________, & _______ weakness
Gynecomastia in 50%
Dysphagia and dysarthria
Widespread ___________
30

Facial, tongue, and proximal

fasiculations
_____________:
Death of upper and lower motor neurons for unknown reasons leading to a progressive loss of the ability to move any of the muscles in the body. Healthy nerves are replaced by hardened tissue
Can be acquired (sporadic) or inherited - mostly sporatic
Amyotrophic Lateral Sclerosis (Lou Gerhig’s Dz)
Sporadic ALS:
80% of all cases of acquired motor neuron disease

Present with -
Painless progressive ________, usually focal then spreading to contiguous muscle groups
Difficulty swallowing, chewing, coughing, and breathing
Muscle atrophy/fasiculations
Spacticity
_______(upper motor neuron signs)
Progressive muscle _______ and weakness (lower motor neuron signs)
weakness

Hyperreflexia

wasting
ALS is a relentlessly progressive disease that culminates in ________ muscle paralysis

_______ is the drug used in treatment of ALS and may delay progression of the disease only slightly

ALS is usually fatal within 3-5 years. Patients with bulbar involvement usually have the ________ prognosis
respiratory

Riluzole

poorest
ALS: Lab and other studies

_______ shows changes of denervation
___ (serum) may be slightly elevated
_____ is normal
Muscle bx

CK

CSF
ALS: Treatment

________ may slow progression of ALS
___________ to help with drooling
Braces and walkers for mobility
PT for contractures, ________ for spacticity
Liquid diet or NG tube feeding for swallowing problems
Consider tracheostomy
Keep patient comfortable in end stages
Riluzole

Anticholinerinergics

diazepam
________ neuropathies one of the most common neuro problems
Can range from mild sensory abnormalities (diabetic neuropathy) to life threatening disorders such as Guillain-Barre syndrome
May be mononeuropathies (CTS) or multiple nerve involvement as seen in Diabetic Neuropathy
Peripheral
Mononeuropathies: Carpal tunnel syndrome

______ nerve compressed at the wrist deep to the flexor retinaculum

Symptoms -
Numbness, tingling, and burning in palm and fingers supplied by median nerve
Thumb, index, middle, medial ½ of ring
Pain and paresthesias mostly at ______, awakening patient
Pain may radiate to forearm and shoulder
Paresthesias relieved by ______ hand
Median

night

shaking
Mononeuropathies: CTS

May persist for years causing sensory loss to fingertips and weakness and atrophy to the ________
______ sign – tapping nerve
______ sign – wrist flexion

Precipitating factors – typing, gardening, house painting, etc
Predisposing factors -
Pregnancy, myxedema, RA
thenar imminence

Tinel’s

Phalen’s
CTS: Dx based on sx and NCS and ___

Treatment:
_______, rest
Injection with __________
______- Sectioning of transverse carpal ligament decompresses the nerve
EMG

Splinting

corticosteroids

Surgery
Mononeuropathies: Ulnar neuropathy (Palsy)

Entrapped ______ nerve due to a poorly healed supracondylar fx with boney overgrowth
Muscle ______ & _______ more a problem than sensory symptoms
Patients complain of atrophy of 1st dorsal interosseous muscle and problems with fine finger movements
May be _______ to small finger and lateral ½ of ring finger
ulner

weakness and atrophy

numbness
Mononeuropathies: __________

Most common pure sensory mononeuropathy
Compression of lateral cutaneous ________ nerve of the thigh as it passes under the inguinal ligament

Sx:
Numbness or burning to lateral ________
Can be provoked by prolonged standing or walking
Usually _______ patients, weight reduction helps
Surgical decompression if evidence of blockage at inguinal ligament
Meralgia Paresthetica

femoral

thigh

obese
Mononeuropathies:
Mononeuritis Multiplex

Seen in patients with DM, RA, Leprosy, polyarteritis nodosa
ie patients who have underlying peripheral neuropathy (polyneuropathy)
Abrupt onset of focal deficit such as _______ or ulnar palsy which is painful
Usually due to ________ of cervical or lumbar plexus
foot drop

ischemia
Mononeuropathies: Bell’s Palsy

Facial paresis of LMN type due to inflammatory reaction of ______ nerve near the stylomastoid foramen

Clinical findings -
Abrupt onset of facial ______, worsening over the following day
____ pain may precedes or occurs with the paresis
Face feels “pulled to one side”
Ipsilateral restriction of eye ______
Disturbance of ______
Hyperacusis due to involvement of fibers to the stapedius
facial

paresis

Ear

closure

taste
Bell’s palsy:
On PE, if the person can raise _____ eyebrows they do not have Bell’s palsy, but a ______ is a possibility
The entire facial nerve is affected before it exits the stylomastoid foramen, so the patient will not be able to elevate the eyebrow
both

stroke
Bell’s Palsy: Treatment

___________is only treatment that may influence outcome
Many clinicians prescribe to all BP patients seen within the 1st 5 days of onset
Some when palsy is complete or severe pain
Treatment _____ mg x 5 days followed by tapering dose over ___ days
Protect ipsilateral eye with lubricating gtts and ________ if closure not possible at night
Surgical decompression procedures are not beneficial
Corticosteroids

60-80

10

eye patch
Polyneuropathies: Guillain – Barre syndrome (acute inflammatory demyelinating polyneuropathy)

Since polio vaccination advent, GBS is most frequent cause of flaccid ________ throughout the world
Presents as weakness or paralysis affecting limbs __________ with loss of muscle stretch reflexes and increased spinal fluid protein without pleocytosis
paralysis

symmetrically
GBS:
Is _______ mediated, following an infectious process in 60% of cases
Seen mostly in with:
Camphylobacter jejuni
Mononucleosis
CMV
Herpes viruses
mycoplasma
immune
GBS: Signs and Sx

Pins and needles sensation in ____ with _______ pain
Weakness within 1-2 days
Mostly in legs, but arms and cranial muscles are 1st to be involved
Muscle _______ reflexes lost early
Weakness progresses rapidly (at peak by 14-30 days)
Critical functions such as _________ can be lost rapidly (days to hours)
Respiratory insufficiency and swallowing difficulty can be life threatening
feet

low back

stretch

respirations
GBS: Treatment

___________ (exchange of patients plasma for albumen) shortens time to recovery
High dose infusion of human __________
Either treatment equally effective, no need to combine them
Plasmapheresis

immunoglobulin
Polyneuropathies: Diabetic Neuopathy

_______ is most frequent cause of neuropathy in the world
Seen in 70% of patients with _________ diabetes
Symptomatic neuopathy affects 5-10% of diabetics
May be symmetrical polyneuropathies or different plexus or nerve injuries
Diabetes

long standing
Polyneuorpathies: Diabetic Neuoropathy

Polyneuopathy is ________ & ________ with sensory loss in _____ (most common)
Prevalence increases with diabetes duration
Can be reduced by maintaining ________ control
distal and symmetric

feet

glycemic
Polyneuropathies: Diabetic neuropathy

Clinical manifestations -
Before sx, PE may show sensation and _______ abnormalities
Sx begin insidiously usually
In some patients, it begin with starting _______
There is elevated pain, vibratory, and thermal threshold causing dysesthesias
Burning, throbbing pain
reflex

insulin
Diabetic neuropathy: DX

Patient with diabetes and clinical picture of neuropathy makes the dx
Can document with electrodiagnostic studies
Should be made only in the setting of _________ diabetes (usually requiring insulin)
Seldom caues ________
long standing

weakness
Diabetic Neuropathy: Treatment

Correction of _______ to as near normal as possible
Painful neuropathy may respond to ____(desipramine) or _________(gabapentin)
blood sugar

TCA’s

anticonvulsants
Disorders of Neuromuscular Transmission: _________

Caused by block of neuromuscular transmission by autoantibodies binding to acetylcholine receptors
Clinically this leads to weakness and easy ________
Myasthenia Gravis (MG)

fatigability
MG:
Occurs at all ages
In association with thymic tumor, thyrotoxicosis, RA, and SLE
Most common in young ______ with HLA-DR3
In older men, most commonly associted with _______
Insidious onset, sometimes discovered by infection that worsens sx
Exacerbates before ______ or during ________
women

thymoma

menses

pregnancy
MG: Signs and Sx

*Present with ptosis, diplopia, dysphagia or difficulty chewing, respiratory difficulty, and/or limb weakness*
Weakness may remain localized or become ________
Sx fluctuate in intensity during the day
Relapses and remissions may last for weeks
Course is slow and progressive and can be fatal due to ________ problems (ex aspiration pneumonia)
generalized

respiratory
MG: PE

Reveals weakness and __________ of affected muscles
EOM’s usually involved causing ______ or ocular palsies with ______ pupils
Bulbar and limb muscles weak
Sustained activity weakens muscles which restrengthen after brief rest
Normal sensation and no reflex changes
fatigability

ptosis

normal
MG:
DX confirmed by response to short acting _________
________ given IV (after test dose) and MG patients will improve stength of weak muscles lasting about 5 minutes
_________ can also be given IM and response lasts for about 2 hours
anticholinergic

Edrophonium

Neostigmine
MG: LAB and other studies

____ can indicate a disturbance of neuromuscular transmission
Assay of serum for increased circulating _______ receptor antibodies (80-90% sensitivity)
EMG

acetylcholine
MG: Treatment

____________ drugs (neostigmine and pyridostigmine)
_________ in all patients under age 60 unless weakness confined to EOM’s
____________ in patients who fail to respond to anticholinesterase meds and have had thymectomy
Last resort is ________ or IV Ig therapy
Anticholinesterase

Thymectomy

Corticosteroids

plasmaphoresis