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Neurology > Neurology intro > Flashcards

Neurology intro Flashcards

1
Q

neurological exam

A

-to identify where the problem is
-right side = think LEFT brain
-lower extremity = medial brain on the motor homonculus -> ACA distribution
-weakness = MOTOR cortex (frontal)

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2
Q

ipsilateral vs contralateral

A

-peripheral facial weakness in upper and lower face (a peripheral 7 nerve palsy) -> ipsilateral to lesion
-hemiparesis is contralateral to lesion of the corticospinal tract above decussation (crossing) of medullary pyramids and ipsilateral to corticospinal tract below decussation

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3
Q

brain stem

A

-mid brain, pons, medulla
-can herniate through foramen magnum if cranial spinal pressure differentials

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4
Q

etiology

A

-Progressive(gradual) onset weakness -> mass (eg, tumor)
-Acute(sudden)- vascular etiology (eg, strokeor transient ischemic attack)
-normal- Sometimes, the history can suggest a particular localization:eg, transient numbness offace/arm/leg suggests involvement of the thalamus, even if the exam is normal.

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5
Q

nasal area

A

-transsphenoidal surgery can be done through sphenoid bone -> brain stem is at risk
-invasive nasal tumors can damage the brain stem

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6
Q

nervous system

A
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7
Q

blood supply to brain

A

-internal carotids supply anterior circulation of the brain -> branches into -> ACA (middle) and MCA (laterals/temporal)
-vertebral artery -> basilar artery -> branches into posterior cerebral artery once reaches brain/pons
-vertebral artery injury -> cerebellum and brain stem damage
-posterior artery damage is more catastrophic than anterior

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8
Q

circle of willis

A

-Circle of Willis=ring-like structure made of the terminal branches of theanterior and posteriorvascularcirculation
Internal carotidsgives rise to:
MCA, ACA andPCoA
-Vertebral artery (PiCA branch to cerebellum) ->Basilar artery ->PCA
-areas of repeated flow
-not a catastrophic event if there is a block
-bilateral destruction of flow can be catastrophic bc no flow to posterior cerebral artery

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9
Q

aneurysms*

A

-MC posterior communication artery (PCOA)
-close to nerve 3
-eye problems present
-starfish appearance
-anterior artery aneurysms are not as severe due to collateral flow

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10
Q

brocas and weineckes areas

A

-left brain

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11
Q

ACA damage

A

-mostly in the legs- loss of strength and sensation
-supplies middle brain

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12
Q

internal capsule

A

-know this
-has motor and sensory fibers
-middle inside part of brain
-face arms and legs symptoms - ACA and MCA stroke (rare) OR tiny stroke in internal capsule!

-damage to internal capsule causes:
-pure motor strokes (MC type of lacunar stroke)
-upper motor neuron signs
-mixed sensorimotor strokes
-face, arms, trunk, leg

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13
Q

brain veins

A

dilated vasculature in the eyes
-arterovenous fistulas -> backup in vessels -> back up into eyes
-increases pressure in veins

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14
Q

CSF

A

-just review
-clear, watery fluid that surrounds the brain and spinal cord
-produced in choroid plexus of the lateral ventricles
-Lateral ventricles -> third ventricle -> fourth ventricle -> subarachnoid space or the central canal of the spinal cord
-Drains into the superior sagittal venous sinus

-high CSF -> hydrocephalus
-can damage brain
-2 types: communicating vs non

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15
Q

ascending tract

A

-from body to head- sensory
-sensory info from leg -> decussates -> brain stem -> thalamus -> cerebral cortex
-lateral spinothalamic tract- pain and temperature
-dorsal columns (posterior funiculi)- deep touch, proprioception, vibratory
-proprioception travels ipsilateral until it hits brain stem and then decussates
-ventral spinothalamic tract- light touch -> numbness

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16
Q

descending tract

A

-from brain to body
-motor
-voluntary
-UMN are in motor cortex of brain
-travel within posterior limb of internal capsule -> anterior brainstem
-90% decussate at junction between medulla of brain stem and spinal cord -> become the lateral tract
-synapse with LMN at anterior horn and exits as peripheral nerve
-

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17
Q

damange to sensory cortex or thalamus will cause…

A

sensory deficits in all 3 types on the contralateral side

-mixed contra/ipsilateral deficits are found in spinal cord damage

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18
Q

numbness

A

-numbness in right leg
-decrease pain and temperature
-if you suspect spinal cord problem -> left spinal cord issue

-vibratory sensation is low but pain and temperature is in tact -> if it is a spinal issue it will be a right side of spinal cord is issue

-if you have decrease pain, temperature, and vibratory -> there is a complete spinal cut

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19
Q

corticospinal tract (pyramidal tract)

A

-between brain and spinal cord- decussates
-90% of time- lateral corticopsinla tract
-synapse with lower motor neuron at the anterior ventral horn

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20
Q

upper lower neuron vs lower motor neuron

A

-UMN injury
-Spastic paralysis- resist fast movement
-No significant muscle atrophy
-Fasciculations and fibrillations are NOT present
-Hyperreflexia- loss of modulation due to loss of UMN
-Babinski reflex may be present

-LMN injury
-flaccid paralysis- floppy no matter what you do
-Significant atrophy
-Fasciculations and fibrillations ARE present
-Hyporeflexia
-Babinski reflex not present
-Weakness is more profound

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21
Q

A patient with a spinal tumor experiences loss of pain-temperature sensation in the left lower extremity, followed by spastic paralysis on the right. Where is the tumor located?

A

-RIGHT ANTEROLATERAL ASPECT OF THE CORD, compressing first the right spinothalamic tract and then enlarging to involve the right corticospinal tract
-upper motor neuron bc spastic

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22
Q

visual system

A

-cerebral hemisphere destruction causes issues to both eyes partially rather than completely contralaterally
-nystagmus- repetitive oscillating movement of eyes
-MC- horizontal jerk nystagmus -> WNL on extreme lateral gaze
-left nystagmus in photo
-vertical nystagmus- abn, brain stem dysfunction/stroke
-bilateral/pendular nystagmus can be congenital or abn brain function

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23
Q

7 elements of the neurologic exam

A

-mental status
-cranial nerves
-motor system
-reflexes
-sensory system
-coordination
-station and gait

-head and hammer, feet like tots, bulk and tone, pretend we fought, stroking, poking, shaking, hot, touch my finger, stand and walk

24
Q

mental status exam hierarchy

A

-from top to bottom
-level of arousal
-attention
-language
-memory
-constructional ability
-higher cognitive functions/praxis

25
Q

level of arousal

A

-Alert
-Lethargic
-Obtunded
-Stuporous

-Comatose
-Definitions vary.
-Strict definition: no motor activity except for posturing and reflex movements.
-Another definition: Glasgow Coma Scale (GCS) < 8

26
Q

glasgow coma scale

A
27
Q

cranial nerves

A
28
Q

olfactory

A

-smell
-goes through cribriform plate -> injury can cause anosmia
-sensory

29
Q

CN2

A

-optic
-sensory
-sees
-afferent visual pathway
-visual field testing, acuity, funduscopic exam (check for papilledema); afferent limb of pupillary response

30
Q

CN 3, 4, 5

A

-ocular motility
-lid and efferent component of pupillary response (specifically constriction)
-LR6, SO4, everything else is 3
-CN3 palsy -> eye looks down and out and dilated

-CN3:
-constriction of pupil
-if injury- dilation
-medial rectus (adduction, superior rectus (elevation), inferior rectus (depression), inferior oblique (up and in), controls levator palpebrae (lid)

-CN4-down and in
-CN5- abducens- lateral rectus (abduction)

31
Q

CN 5

A

-trigeminal
-chews
-sensation of face

-motor- V3
-anterior- temporalis, internal and external ptyerygoid, masseter
-posterior- mylohyoid, digastric

-sensory- face
-V1- ophthalmic- forehead, eye, upper nose, anterior scalp
-V2- maxillary- cheek, lower nose, upper lip
-V3- mandibular- posterior scalp, chin, teeth, inner cheek, lower lip, anterior 2/3 tongue

-corneal reflex- afferent component, use cotton wisp

32
Q

CN7

A

-moves face
-salivates
-cries
-motor- frontalis, orbicularis oculi, orbicularis oris, corneal reflex
-anterior 2/3 tongue (taste)
-smile/show teeth/close eyes tightly

33
Q

vestibulocochlear

A

-CN8
-hearing and vestibular function
-balance

34
Q

CN 9

A

-glossopharyngeal
-taste posterior 1/3
-salivates
-swallows
-monitors carotid sinus
-afferent- gag reflex
-pull uvula ipsilateral*
-right CN9 palsy will cause uvula to deviate contralaterally

35
Q

CNX

A

-vagus
-taste
-swallow
-cough
-lifts palate
-talks
-communicates with thoraco-abdominal viscera (decrease HR, breathing, digestion)
-sensory- external auditory meatus
-efferent component of gag reflex

36
Q

CN11

A

-accessory
-turns head and lifts shoulders
-trapezius (shoulder shrug)
-sternocleidomastoid (turning head laterally)

37
Q

CN12

A

-hypoglossal
-moves tongue
-pushes tongue contralaterally
-right CN12 palsy -> tongue deviates to right

38
Q

normal pup size

A

-3-5mm

39
Q

case

A

-PCOA aneurysm

40
Q

A 50-year-old female with no past medical history presents to the ED with a diffuse, constant headache onset a few weeks.Droopiness of the left eye occasional double vision. Right eye exam normal with 3mm pupil
LEFT EYE EXAM:
ptosis
inability to adduct left eye, ability to abduct
Pupil is dilated at 5mm and minimally reactive to light
The remaining cranial nerve testing and components of the neurological exam are normal.

A

-CN3, oculomotor palsy
-ptosis- inactivation of levator palpebrae
-mydriasis- decreased tone of contrictor pupillae muscles
-down and out- unopposed left superior oblique and lateral rectus

-cause?:
-usually microvascular etiology (pupil will be spared)
-if pupil is involved consider- trauma, aneurysm, tumor

41
Q

horner syndrome

A

-sympathetic nerve problem
-TRIAD:
-1. PTOSIS- superior tarsal muscle requires sympathetic innervation to keep eyelid retracted
-2. MIOSIS (pupil constriction)- loss of sympathetic input causes unopposed parasympathetic -> contriction
-3. ANHIDROSIS- loss of sympathetic activity -> pattern of anhidrosis can help locate lesion
-if no sweating on entire face -> tension at level of carotid artery
-partial anhidrosis on medial forehead ipsilateral side of nose -> lesion distal to carotid bulb

-causes:
-carotid artery dissection**
-PICA or vertebral artery occlusion- stroke
-pancoast tumor, nasopharyngeal tumors
-lymphoproliferative disorders
-brachial plexus injury
-cavernous sinus thrombosis
-fibromuscular dysplasia
-marcus gunn pupil

42
Q

fixed pupils

A

-midbrain lesions
-not good

43
Q

motor

A

-corticospinal tract- from betz cell in cerebral cortex to anterior horn cell in spinal cord

-power:
-5 full normal power against resistance
-4 moves against some resistance of examiner
-3 moves against gravity
-2 active joint movement with gravity removed (eg, moves leg along surface of bed)
-1 muscle contraction seen, but no movement at joint
-0 no muscle contraction seen
-anything less than 5 is significant

-tone:
-resistance felt when joint moved passively
-normal, flaccid, increased, spastic

-involuntary movements (fasciculations, tremor, myoclonus, etc)

-patterns of weakness*
-Face/arm/leg symmetrically (usually subcortical/brainstem) or
-Face and arm > leg (MCA distribution) or
-Monoparesis (usually cortical)
-Symmetrical proximal (myopathy)

-Most important to test: Proximal and distal
-In upper extremity, deltoid and fine finger movements
-In lower extremity, hip flexors and ankle dorsiflexion

44
Q

sensory

A

-light touch
-pain and temp:
-testing pain- break off part of cotton tipped applicator
-testing cold- use handle of tuning fork or ice in glove

-joint position sense (JPS)- move great toe (small excursion)
-vibration- 128 Hz tuning fork
-graphesthesia- ability to identify writing on hand
-stereognosis- ability to discriminate coins placed in palm when eyes closed

45
Q

reflexes

A

-0 (absent)
-1+ hyporeflexia
-2+ Normal
-3+ increased (seen in upper motor neuron disease)
-4+ clonus -> continuous movement back and forth

-Babinski (extensor plantar response) indicates corticospinal tract lesion (anywhere along its course)

-S1,S2- buckle my shoe - ACHILLES
-L3,L4- kick the door- PATELLAR
-C5,C6- pick up sticks- BICEPS/BRACHIORADIALIS
-C7,C8- lay them straight- TRICEPS

46
Q

hyporeflexia

A

-Decreased reflexes can be due to impaired SENSORY input or MOTOR output or pt apprehension
-Can be present in LMN lesions, including nerve root lesions with radiculopathy and peripheral nerve lesions or polyneuropathies
-Look for associated weakness, decreased muscle tone (flaccidity), fasciculations, and atrophy
-Possible causes: Diabetes, hypothyroidism, spinal cord injury or compression, cerebellar disease, GBS
-Isolated AREFLEXIA is most commonly the result of a root lesion, a peripheral nerve injury or entrapment, or a mononeuropathy

47
Q

hyperreflexia

A

-Enhanced reflexes can be associated with an upper motor neuron lesion / CNS disease (e.g. stroke or spinal cord injury)
-Look for increased muscle tone (spasticity), weakness, +Babinski
-Clonus, if present, is never a normal finding.
-Hyperthyroidism a/w hyperreflexia
-Increased reflexes can be normal, especially if bilateral.
-Children frequently have exaggerated reflexes (more prominent in upper extremities)

48
Q

cerebellum decussation

A

-double decussation
-always ipsilateral problems
-cerebellar disease -> stroke, cerebritis, metabolic insults -> awkwardness of intentional movement on ipsilateral side

49
Q

signs of cerebellar disease

A

-awkwardness of intentional movement on ipsilateral side
-scan speech- brit-ish par-la-mant
-ataxia -> acute cerebellar ataxia- wide based and staggering gait with tendancy to fall to same side of lesions
-poor coordination of movement
-dysmetria- past pointing or overshooting ex. fails finger to nose or heel to shin
-dysdiadochokinesia- falling rapid alternating movement test (feet, finger tapping)
-decreased tendon reflex of affected side
-asthenia- muscles tire more easily than normal
-INTENTION TREMOR
-nystagmus- fast phase toward cerebellar lesion
-not that romberg test is NOT sign of cerebellar disease (it is proprioception problem (posterior column))

-appendicular ataxia- lateral cerebellar hemisphere
-truncal axtaxia- vermian (midline)

50
Q

basal ganglia disorders

A

-symptoms can be divided into 2 classes:
-1. DYSKINESIAS- abnormal, involuntary movements
-Resting tremors: body parts will display a 4-7 Hz tremor that stops moving (Ex. Pill rolling of Parkinson’s)
-Athetosis- involuntary, writhing movements, especially of hands and face
-Chorea- continuous, writhing movements of entire body. extreme form of athetosis. (Ex: Chorea of Huntington’s disease)
-Ballismus- involuntary, ballistic movements of extremities
-Tardive dyskinesia- result from long-term use of antipsychotics that target dopamine -> involuntary movements of tongue, face, arms, lips, and other body parts.

-2. Akinesias: abnormal, involuntary postures
-Rigidity- resistance to passive movement of limb
-Unlike spasticity, rigidity doesnt depend on speed of passive movement
-resistance can be so great it is referred to as lead-pipe rigidity, because moving limb feels like bending a lead pipe.
-can be coupled with tremors -> called cogwheel rigidity -> moving limb feels like catching and release of gears.
-Dystonia- involuntary adoption of abnormal postures, as agonist and antagonist muscles both contract and become so rigid that pt cant maintain normal posture.
-Bradykinesia - slowness

-Because the basal ganglia were once considered to form a separate, “extrapyramidal” motor system, these symptoms are called extrapyramidal disorders

51
Q

trigeminal neuralgia (tic doleroux)

A

-Compression ofCNV
-causes:Superior cerebellarartery, pons AVM,MS,Acoustic neuroma,glioblastoma,Lyme disease
-Severe, unilateral, stabbing, shooting pain ina trigeminal nerve distribution(usually V2/V3)
-worse with chewing and talking
-Pain paroxysms lasts several seconds
-Tender to palpation over maxilla/mandible
-Ages 50-70, F»M
-DX:Clinical, though CT/MRI may identify acompressive cause
-TX:Carbamazepine (Tegretol), gabapentin,baclofen
-Surgery:Microvascular decompression, neuro-ablation

52
Q

bell’s palsy

A

-LMN weakness of CN7
-idiopathic- usually viral related ischemia/demyelination (herpes zoster, HSV, EBV, lyme disease)
-unilateral total facial weakness that evolves over 48 hrs
-eyebrows sag (cant wrinkle forehead), eyes wont close, mouth corner droops, decreased tears, hyperacusis (decreased sound tolerance), agnusia (decrease taste)
->50 years old, diabetes, 3rd trimester pregnancy
-dx- clinical, EMG,NCV, if longer than 3 weeks
-tx- corticosteroids within 3-4 days of onset
-complications- corneal exposure causing keratitis, incomplete recovery
-prognosis- 90% resolve in 3 weeks to 6 months

53
Q

gait

A

-Assess their base, stride, and tandem gait
-Types of abnormal gait:
-Ataxic: wide-based, irregular
-Shuffling, short steps: parkinsonian
-Spastic: stiff legged, scissoring

-Romberg test:
-Have pt stand feet together, arms at sides -> have them close their eyes.
-Positive Romberg’s sign: Pt begins to sway or fall once eyes close
-balance requires 2/3 sensory inputs: visual, vestibular and proprioceptive
-if loss of visual input causes swaying -> one more must be missing!
-May be due to lesion of dorsal columns or other loss of significant sensory or spinovestibular feedback.
-“Pull test”- pull them backwards, they must keep balance by using one foot to stabilize position

54
Q

imaging

A

CT = Computed tomography
Shows brain but not in detail, good for large bleeds, strokes, lesions, or masses
Pros: Faster, cheaper, less sensitive to patient motion, better for bony details, can be used despite metal in body (implantable medical devices)

MRI = Magnetic resonance imaging
Painless, non-invasive method that produces 3D black-and white imaging of the brain and/or spinal cord.
Pros: Better for soft tissue visualization, no radiation, more sensitive for abnormalities.
Cons: Time-consuming, claustrophobia inducing, magnet

PET scans =Positron Emission Tomography
Good for seeing metabolic changes in the brain
Reveals the functionality of tissues and organs utilizing radioactive tracers that bind to glucose in the body
Often used for dementia, seizures, tumors, brain damage from trauma

55
Q

electrophysiological tests

A

EEG = Electroencephalogram
Measures electrical activities of the brain from electrodes placed on the scalp
Can be used to aid diagnosis of seizures/epilepsy, brain damage from head injuries, sleep disorders

EMG = Electromyography
Measures how well muscles respond to electrical signals emitted to motor nerves
Needle electrode is inserted into a muscle, pt is asked to contract the muscle, response is recorded
Diagnostic tool in the evaluation of pain, weakness, sensory disturbance, fatigue and atrophy
Should always be performed with a NCS below

NCS = Nerve conduction studies
Measures how well the nerves sends signals from your brain to muscle
Electrical pulses are applied to the nerves, and we record the time it takes for transmission of signal to a disc electrode on the skin distal to the signal

-EMG + NCS = peripheral neuropathy, motor neuron disease (ALS), myopathies, neuromuscular junction disorders

Neurology (11 decks)

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