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177 Cards in this Set

  • Front
  • Back

gray matter vs white matter

gray: aggregations of neuronal cell bodies; rims the surfaces of the cerebral hemispheres forming the cerebral cortex
white: neuronal axons that are coated with myelin
internal capsule
white-matter structure where myelinated fibers converge from all parts of the cerebral cortex and descend into the brainstem
reticular activating system
in the diencephalon and upper brainstem; consciousness depends on this
spinal cord termination
L1/L2
where are lumbar punctures performed

L3/L4 or L4/L5


corticospinal (pyramidal) tract

mediate voluntary movement and integrate skilled, complicated, or delicate movements by stimulating selected muscular actions and inhibiting others
- carry impulses that inhibit muscle tone
- originate in motor cortex
- travel down into lower medulla where they decussate at pyramids
- cross in medulla and go downward
** tracts that synapse in the brainstem with motor nuclei of cranial nerves= corticobulbar

bradykinesia

damage to basal ganglia
- slowness or lack of spontaneous and automatic movements
pain and temperature
pass into the posterior horn of the spinal cord and synapse with secondary neurons
crude touch fibers
pass into posterior horn and synapse with secondary neurons
-secondary neurons cross to opposite side and pass upward in spinothalamic tract into the thalamus

position and vibration fibers

pass directly into posterior columns of the cord and travrel up to medulla with fibers of fine touch
-synapse in medulla with secondary neurons
- fibers from secondary neurons cross to opposite side at medullary level and continue on to thalamus

thalamic level

quality of sensation is perceived but fine distinctions are not made

loss of position and vibration sense with preservation of other sensations- where is the lesion?

posterior columnstransection of the spinal cord

all componenets of a reflex arc

sensory nerve fibers
spinal cord synapse
motor nerve fibers
neuromuscular junction
muscle fibers

ankle reflex
S1
knee reflex
L2-4
brachioradialis reflex
C5-6
biceps reflex
C5-6
triceps reflex
C6-7
abdominal reflex (upper)
T8-10
abdominal reflex (lower)
T10-12
plantar reflex
L5-S1
anal reflex
S2-4
different presentation of myopathy vs polyneuropathy
b/l proximal weakness in myopathy
b/l distal wekaness in polyneuropathy
presentation of paresthesias around the mouth and in hands Ddx?
hyperventilation
dysesthesias
distorted sensation in response to a stimulus (light touch or pinprick as burning or tingling sensation)
vasovagal syncompe
emotional stress and warning symptoms (flushing, warmth, nausea); slow onset, slow offset
cardiac syncope
arrhythmias, sudden onset/offset
presentation of tonic-clonic motor activity, bladder or bowel incontinence, and postictal state
generalized seizure; may bite tongue
stroke
sudden neurologic deficit caused by CV ischemia (80-85%) or hemorrhage (15-20%)
hemorrhagic strokes- two types
intracerebral (10-15%) or subarachnoid (5%)
TIA
sudden focal neurologic deficit- lasting less than 24 hours- more recent: less than 1 hour without underlying structural defects
predictive value of TIAs
15% of patients progress to stroke w/i first 3 months
when is risk of stroke highest
first 30 days after TIA
middle cerebral artery occlusion symptoms
visual field cuts and contralateral hemiparesis and sensory deficits
MCA occlusion in L hemisphere
aphasia
MCA occlusion in R hemisphere
hemineglect
most common cause of hemorrhagic stroke from subarachnoid hemorrhage
rupture of saccular aneurysms in circle of Wilils
ideal level of HgA1C in diabetics to control risk for stroke
< 7.4% so onset of neuropathy drops by 50-60%
loss of sense of smell indicates
sinus congestion, head trauma, smoking, aging, use of cocaine, parkinsons
disc pallor vs disc bulging
pallor: optic atrophy
bulging: papilledema
prechiasmal, anterior defects (visual)
glaucoma, retinal emboli, optic neuritis
bitemporal hemianopsias
defects at optic chiasm- pituitary
homonymous hemianopsias or quadrantanopsia
postchiasmal lesions- parietal lobe- acuity normal
monocular diplopia
local problems with glasses or lenses, cataracts, astigmatism, ptosis
binocular diplopia
CN III, IV, VI, neuropathy (40%), MG, trauama, thyroid ophthalmopathy, INO (muscle disease)
nystagmus (define and when you see it)
involuntary jerking movement of the eyes with quick and slow components
- cerebellar disease (increases with retinal fixation), vestibular disorders (decreases with retinal fixation)
how is nystagmus named
for the direction of the fast component
unilateral weakness in CN V pontine lesions
b/l weakness in cerebral hemispheric disease because of b/l cortical innervation
ipsilateral face but contralateral body sensory loss localizes lesion to?
brainstem
acoustic neuroma presentation
absent blinking and sensorineural hearing loss
conductive vs. sensorineural hearing loss
conductive: impaired air thorugh ear transmission
sensorineural: damage to chochlear branch of CN VIII
Rinne vs Weber test
Rinne: air and bone conduction- normal air > bone- conductive- bone longer than air in affected ear- sensorineural- air longer than bone but less than 2:1 ratio
Weber: lateralization- normal NONE- conductive- lateralization of deaf ear
sensorineural- lateralization to better ear
causes of conductive hearing loss
cerumen, otosclerosis, otitis media
b/l lesion of vagus nerve
failure of palate to rise
u/l lesion of vagus
one side doesnt rise and with uvula is pulled toward normal side
tongue atrophy and fasciculations
amyotrophic lateral sclerosis, polio
unilateral cortical lesion

protruded tongue deviates transiently in a direction away from the side of cortical lesion, toward side of weakness

pseudohypertrophy and when seen
increased bulk with diminished strength: DMD
sign of atrophy in the hands
flattening of thenar and hypothena eminences and furrowing b/w metacarpals; median and ulnar nerve damage, respectively
weakness of extension
peripheral nerve disease such as radial nerve damage and in CNS disease producing hemiplegia- stroke/MS
weak grip (C7-T1)

cervical radiculopathy, de Wuervain's tenosynovitis, CTS, arthritis, epicondylitis

weak finger abduction
ulnar nerve disorders
weak opposition of the thumb
medial nerve
flexion of hip tests
L2-L4; iliopsoas
signs of cerebellar disease
ataxia, nystagmus, dysarthria, hypotonia
dysdiadochokinesis
when one movement cannot be followed quickly by its opposite; movements are irregular, slow, clumsy- cerebellar disease
dysmetria
finger initially overshoots but eventually reaches it
differentiation of ataxia from dorsal column disease vs cerebellar disease
cerebellar: difficulty standing with feet together whether eyes are open or closed
-those with dorsal column problems compensate by eyes then demonstrate (+) romberg sign
pronator drift
sensitive and specific for corticospinal tract lesion originating in contralateral hemisphere
stereognosis, number identification, two-point discrimination impaired in?
posterior column disease
astereognosis
inability to recognize objects placed in hand
-suggest lesion in sensory cortex

what presents with lesions in sensory cortex

astereognosis, inability to recognize numbers (graphesthesia), increase distance between two recognizable points, impairs ability to localize points accurately



-only one stimulus will be recognized--sensation on opposite side of the damaged cortex is gone

neck stiffness and resistance to flexion in what perfect of pts with acute bacterial meningitis vs subarachnoid hemorrhage
90%- meningitis
20-85%- subarachnoid hemorrhage
Brudzinski's Sign
flex the neck; watch the hips and knees- positive when hips and knees flex
Kernig's Sign
flex the leg at both hip and knee then straighten- pain and increased resistance to extending the knee- (+) Kernig's sign- b/l indicates meningeal irritation
positive straight leg test?

pain radiating into ipsilateral leg indicating lumbosacral radiculopathy, sciatic neuropathy, or both

sensitivity and specificity of straight leg raise for disc herniation vs crossed straight-leg raise
95% and 25%
40% and 90%
asterixis

sudden, brief, nonrhythmic flexion of hands and fingers- liver disease, uremia, hypercapnia

winging of scapula

weakness of serratus anterior (seen in MD) / long thoracic nerve

*Five clinical signs that stronly predict death in coma
absent corneal response, absent pupillary response, absent withdrawal response to pain, no motor response; at 72 hours-no motor response
DONTS when assessing comatose patient
1.) don't dilate the pupils! (most important clue to underlying cause of coma [structural vs. metabolic])
2.) don't flex the neck if there is any question of trauma to the head or neck
-immobilize C-spine and get an x-ray first
structural hemispheric lesions (eye direction)
look at the lesion in the affected hemisphere
comatose pt with lack of doll's eye movements

-ability to move both eyes to one side is lost--> lesion of midbrain or pons

hemiplegia of sudden cerebral accidents
flaccid at first causing limp hand drops to form a right angle with the wrist
movement of flaccid leg in acute hemiplegia
falls fast into extension with external rotation at hip
mechanism of acute ischemic stroke
-ischemic brain injury begins with a central core of very low perfusion and often irreversible cell death
-core surrounded by ischemic penumbra of cells that could be salvaged
most irreversible damage occurs when
3-6 hrs after onset of symptoms
NAME THAT STROKE! contralateral leg weakness
ACA
NAME THAT STROKE! contralateral face, arm>leg weakness, sensory loss, field cut, aphasia (L lesion), neglect/apraxia (R lesion)
anterior circulation of MCA
NAME THAT STROKE! contralateral motor or sensory deficit without cortical signs
subcortical circulation- leticulostriate deep penetrating branches of MCA
four common syndromes of lacunar infarcts
1.) pure motor hemiparesis
2.) pure sensory hemianesthesia
3.) ataxic hemiparesis
4.) clumsy hand-dysarthria syndrome
NAME THAT STROKE! contralateral field cut
posterior ciruclation- PCA
NAME THAT STROKE! cortical blindness but preserved pupillary light reaction
b/l PCA infarction
NAME THAT STROKE! dysphagia, dysarthria, tongue/palate deviation and/or ataxia with crossed sensory/motor deficits (ipsilateral face/contralateral body)
posterior circulation- brainstem, vertebral, basilar artery branches
NAME THAT STROKE! oculomotor deficits and/or ataxia with crossed sensory/motor deficits
posterior circulation- basilar artery
decerebrate rigidity (abnormal extensor response)
-jaws clenched, neck extended, arms adducted and stiffly extended at elbows, forearms protonated, wrists/fingers flexed
- legs extended at the knees, feet plantar flexed
- may occur spontaneously
**lesion in diencephalon, midbrain, or pons
**also from severe metabolic disorders- hypoxia or hypoglycemia
hemiplegia (early)
-flaccid (later spastic)
- paralyzed arm and leg slack- fall loosely
- leg may lie externally rotated
- if lower face paralyzed, cheek puffs out with exhalation
- both eyes away from paralyzed side
decorticate rigidity (abnormal flexor response)
- upper arms flexed tight to the sides with elbows, wrists, fingers flexed
- legs extended and internally rotated
- feet are plantar flexed
- lesion of corticospinal tracts w/i or near cerebral hemispheres
bilaterally small pupils
1.) damage to sympathetic pathways in hypothalamus
2.) metabolic encephalopathy
- light rxns normal
pinpoint pupils (<1 mm)
1.) hemorrhage in pons
2.) morphine, heroin, narcotics
midposition fixed pupils
midposition of slightly dilated (4-6mm)- damage in midbrain
b/l fixed and dilated pupils
severe anoxia and its sympathomimetic effects
- atropinelike agents, phenothiazines, TCAs
b/l large reactive pupils
cocaine, amphetamine, LSD, sympathomimetics
one large pupil (fixed and dilated)
herniation of the temporal lobe (compression of CN III and midbrain)

features of toxic-metabolic coma

*arousal centers poisoned or critical substrates depleted*
- regular respiration: normal or fast; irregular: Cheyne-Stokes
-pupils: equal, reactive- may be unreactive if fixed and dilated from anticholinergics/hypothermia
- level of consciousness changes after pupils change

causes of toxic-metabolic coma
uremia, hyperglycemia, alcohol, drugs, liver failure, hypothyroidism, hypoglycemia, anoxia, ischemia, meningitis, encephalitis, hyperthermia, hypothermia
features of structural coma
*lesion destroys or compresses brainstem arousal areas*
- irregular respiration (Cheyne-Stokes or ataxic)
- pupils: unequal or unreactive- midbrain compression if midposition and fixed
- if dilated and fixed- compression of CN III
- level of consciousness changes before pupils change
causes of structural coma
epidural, subdural, intracerebral hemorrhage, cerebral infarct or embolus, tumor, abscess, brainstem infarct, tumor, hemorrhage, cerebellar infarct, hemorrhage, tumor or abscess
steppage gait
- foot drop
- cannot walk on heels
- tibialis anterior and toe extensors are weak
parkinsonian gait
- basal-ganglia defects
- posture is stopped (flexion of head, arms, hips, knees(
- fenestrating
- poor postural control (retropulsion)

cerebellar ataxic gait

staggering, unsteady, wide based
- cannot stand with feet together regardless of eyes

sensory ataxia

- gait unsteady, wide based
- pts throw feet forward and outward and bring them down, first on heels then toes

this suggests progressive subacute onset of distal lower extremity weakness

guillan barre syndrome

what indicates an abrupt onset of motor and sesory deficitis

TIA or stroke

ataxia, diplipa, and dysarthria indicate

vertebrobasilar TIA or stroke also consider posterior fossa tumor and vertebrobasial or hemicranial migraine

this suggests chronic more graduate, onset of weakness in lower extremities

metastatic cord lesions and lumbar disc disease

central focal or asymmetric weakness suggest

ischemic, thrombotic, or mass lesions

peripher focal or asymmetric weakness sugest

nerve injury to the NMJ, to myopathies or intrinsic muscle diseases

proximal limb weakness usually symmetric and without sensory loss suggests

myopthaties from alcohol, drugs like glucocorticoids, and inflammatory muscle disorders (myosities and dermatomyositis)

proximal typically asymmetric weakness that gets worse with effort and associated with bulbar symptoms lke diplipa, ptosis, and dysarthria, and dysphagia suggest..

myasthenia graves

sensory changes that arise from local nerve compression or entrapment in hand numbness suggests a problem with..

medial, ulnar, or radial nerve

sensory changes in nerve root compression suggest..

issues with dermatomal sensory loss from vertebral bone spurs or herniated discs or central lesions from stroke or MS

diabetic with burning pain suggests..

sensory neuropathies

behavioral risk factors for ischemic stroke

1. hypertension


2. dislipedemia


3. weight


4. exercise


5. smoking


6. alcohol use

top contributing factors for stroke

1. AA


2. HTN


3. diabetes


4. left ventricular hypertrophy


5. income and insurance gaps

what are stroke warning signs

numbness/weakness; confusion/trouble speaking; trouble seeing and walking; dizziness; balance problems; severe headache

early predictions of stroke

ABCD2


a=age >60


b=BP >140/90


c=clinical features--focal weakness or impaired speech


d=duration--up to >60min


d=diabetes

common causes of acute symptomatic seizures

1. head trauma


2. alcohol


3. cocaine


4. w/drawal from alcohol, benzos, and barbs


5. metabolic issues like low gluc, low Ca, low Na


6. stroke


7. meningitis


8. encephalitis


what suggests parkinsons disease

-low frequency unilateral resting tremor


-rigidity


-bradykinesia (slow movement)

this is high-frequency, bilateral, upper extremity tremor, with both limb movement, and sustained posture, w/ possible head, voice, and leg tremors present

essential tremors

what are disease specific risk factors for stroke

1. atrial fib


-CHADS2


--c=CHF


--h=HTN


--a=age >75


--d=diabetes


--s=prior stroke or TIA



2.carotid artery disease

categories for ischemic stroke

-large artery atherosclerotic infarction


-cardiac embolism


-small vessel lacunar disease


-dissection


-hypercoagulable states


-paradocial embolism through foramen ovale

most comon diabetes peripheral neuropathy

distal symmetric sensorimotor polyneuropathy


(burning electrical pain in lower extremities at night)

five categories for a comprehensive or screening neuro exam

1. mental status, speech, language


2. CN


3. motor-coordination, gait, and strength


4. sensory-light, temp, touch, vibrations, discrimination


5. reflexes-DTR and plantar responses

loss of smell can occur in..

sinus conditions, head trauma, smoking, aging, cocaine use, and PD

large pupil reacts poorly to light or aniscoria worsens in light and large pupil has abnormal pupillary constriction..this is seen in..

CN 3 palsy

if pt awake and if ptosis and opthalmoplegia also present with anisocoria then consider...

intracranial aneurysm

if pt in coma, with ptosis and opthalmoplegia also present with anisocoria then consider...

transtentorial herniation

binocular diplopia suggests...

CN3, 4, and 6 neuropathies (40% of patients) and eye muscle diseases (MG, trauma, thyroid opthalmopathy, and internuclear opthalmoplegia)

involuntary jerking movements of the eyes with quick and slow components

nystagmus

how is nystagmus named

for the direction of the quick component (horizontal, vertical, mixed, or rotary)

nystagmus presents in what kind of diseases

Cerebellar disease, like gait ataxia and dysarthria and vestibular disorders and internuclear opthalmoplegia

CN 5 carries which blinking reflex

sensory limb

CN 7 carries which blinking reflex

motor response

what portion of face does a peripheral injury (CN7) affect and an example

Bells palsy


-both upper and lower face

what portion of face does a central lesion affect

mainly lower b/c upper face will receive upper motor neurons from opposite side of face

loss of taste, hyperacusis, and increased or decreased tearing is seen in...

bells palsy

hypertrophy

increased muscle bulk with proportionate strength

lesion to corticospinal tract causes and what is a common cause

-spascity (hypertonia=increased muscle tone)


--common cause: stroke

basal ganglia

-controls muscle tone and controlled body movements (walking)

lesion to basal ganglia would result in and a common cause

-rigidity (increased resistance, esp during ROM)


--common cause=parkinsons

lead pipe rigidity

-increased resistance that persists throughout the movement arc and independ of rate of movement

cogwheel rigidity

with flexion and extension of the wrist or forearm, a superimposed ratchetlike jerkiness

paresis

impaired strength (weakness)

paralysis or plegia

absence of strength

hemiparesis

weakness to one half of the body

paraplegia

paralysis of the legs

quadriplegia

paralysis of all four limbs

what is a grade 0 on the muscle strength scale

no muscular contractions detected

what is a grade 5 on the muscle strength scale

normal muscle strength

inability to heel walk is a sensitive test for...

corticospinal tract damage

disease example of loss of vibration sense in posterior column disease

tertiary syph and vit B 12 deficiency

disease examples of loss of position sense in posterior column disease

MS, tabes dorsalis, vit B 12 deficiency, and peripheral neuropathy from DM


reflex

involuntary sterotypical response that involves at least one afferent and one efferent across a single synapse

all componenets of a reflex arc

sensory nerve fibers
spinal cord synapse
motor nerve fibers
neuromuscular junction
muscle fibers

CNS lesion along descending corticospinal tract is..

hyperactive reflexes (hyperflexia)

other associated upper motor neuron findings of hyperactive reflexes are...

weakness, spasticity, or a positive Babinski

hypothyroidism is seen and felt where..

ankle reflexes

what does sustained clonus indicate

CNS disease

abdominal reflexes are absent in....

CNS and PNS disorders

loss of S2-4 anal reflex suggests..

cauda equina lesion

subarachnoid space inflammation will cause resistance in....

-nuchal flexion (neck); brudzinski (femoral n.); and kernigs signs (sciatic n.)

sciatica is 5x more likely when...

-confirm ipsilateral calf wasting


-weak ankle dorsiflexion


how does lethargic pt look

-drowsy, opens eyes and responds, falls back to sleep

how does obtunded pt look

-opens eyes, responds slowly, somewhat confused


-alertness and interest in environment decreased

how does a stuporous pt look

-painful stimuli needed


-verbal response slow or absent


-unresponsive when stimuli ceases


-minimum awareness of self or environment

how does comatose pt look

-unarousable and eyes closed