Nervous System Flashcards
Four Brain Regions
Cerebrum: frontal, parietal, temporal, occipital
Diencephalon-Thalmus, Hypothalmus and basal ganglia
Brainstem- Midbrain, Pons, Medulla
Cerebellum
Brain Tissue
Gray- formed by collection of erve cell bodies
White- myelin coated axons
Internal capsule- where all myeinated fibers from cerebral cortex converge and descend into brainstem
Diencephalon
Thalmus(sensory impulses relay to cerebral cortex) Hypothalmus( homeostasis- reg HR,BP, Temp also endocrine, emo behavior. Hormones excreted from hypothalmus directly affect pituitary) basal ganglia(affect movement)
Thalmus vs Internal Capsule
Thalmus bus stop for all sensroy impulses going into brain, Internal capsule bus stop for all sensory impules going out of brain
Consciousness
interaction between cerebral hemispheres, diencephalon, upper brainstem, RAS
Cerebellum
base of brain, coordinates movement, maintains upright position
Spinal Cord
C1-8 T1-12 L1-5 S1-5 C
Cauda Equina
Spinal cords ends at L1-2, then the lumbar and sacral roots fan out like horse tail
Lumbar puncture
done L3-4 or L4-5
CN 1-12
On old olympus towering tops a finn and german viewed some hopps
CN can be motor, sensory or both
Some say marry money but my brother says big breasts matter more
Nerve Roots
Ant root- motor/efferent
Post root- sensory/afferent
Upper motor neurons
cell bodies originate in brain and spinal cord. UA to leave CNS, must synapse with lower motor neurons, which carry message to muscle/rest of body
Lower motor neurons
cell bodies located in brain stem, but axons can leave CNS to synapse with muscles- These are cranial/spinal nerve
Motor: Corticospinal (pyramidal) tract
mediate voluntary movement by stim muscle action and inhibiting others. Carry impulses that inhibit muscle tone. Originates in motor cortex of brain. Motor fiber travels down lower medulla, cross to opposite side of medulla, cont down, syn with ant horn/immediate neurons.
Corticobulbar
tracts synapsing in brainstem with motor nuclei of CN
Motor: Basal Ganglia System
complex system includes motor pathway between cerebral cortex, basal ganglia, brainstem, spinal cord. Maintains muscle tone and control body movements
Motor: Cerebellar System
receives sensory/motor input and coordinates motor activity, maintains equilibrium, helps control posture.
Movement
Voluntary- Cortex
Automatic- basal ganglia
reflex sensory- sensory receptors.
Higher motor pathways
affect motor mvmt only through lower system- translates into sction in ant horn. Lesion in any areas- will affect mvmt or reflex activity
Upper vs Lower motor neuron damage
Upper- inc muscle tone/DTR
Lower- dec muscle tone/DTR
Damage to Basal Ganglia
inc muscle tone, diturbs posture/gait, bradykinesia, invol mvmt
Damage to Cerebellum
dec muscle tone, imp coordination/gait & equilibrium
Nystagmus, dysarthria, hypotonia and ataxia
Sensory Pathways
reflex activities, conscious sensation, body position, reg ANS(HR,BP,RR), relays impulses from skin/mucous membranes/ tendons/ viscera, reg sensation of pain/temp/position/touch.
Sensory: Spinothalmic Tract 1
from neuron to post horn, synapse with secondary neurons- cross to opposite side and travel up to thalmus (Pain, temp, crude touch-light touch not localized)
Sensory: Spinothalmic Tract 2
sensations of vibration/position/fine touch(with localization)- pass directly into post horn- travel up to medulla with secondary sensory neurons, cross to opposite side at medullary level and cont to thalmus.
Thalmic Level
Quality of sensation perceived, fine distinction not made
Sensory Cortex
Full perception, localization, high order discrimination made
Sensory Cortex Lesions
may not impair perception of pain/touch/ position but will impair finer discrimination.
Cannot appreciate size/shape/texture of object by feel.
Proprioception
sense of mvmt, body position independant of vision. Gained from input of sensory nerve terminals in muscles/tendons/joints/vestibuar apparatus
Loss of position sense- tabes dorsalis, MS, B12 def from post colum disease, PN form DM
Dermatome
band of skin innervated by sensory root of a single spinal nerve
Sensory level may be several segments below injury- reason unknown
DTR
tap on tendon, activates special sensory fibers, trigger sensory impulse to spinal cord via peripheral nerve synapses directly with ant horn innervating same muscle, crosses NM junction, muscle contracts, completes reflex arc
HH c/o
HA, dizzy, vertigo, weakness, numbness, abn/loss of sensation, LOC, syncope/near-syncope, Sz, tremors/invol mvmt
HA
Ask: severity, location, duration assoc Sx like visual, wkns, loss of sens. Affected by sneezing, coughing or suddent mvmt of head- which can inc ICP
SAH- worst HA of life
Meningitis- severe HA
Mass lesions/absess- dull HA in same location
Dizzy
what experienced, light headed/faint, room spining/rotating
Light-headedness in plapitations, near syncope from VV stim, low BP, febile, or others.
Vertigo- inner ear, brainstem tumor.
Elderly- meds may contribute
Assoc Sx- diplopia, dysarthria, ataxia- may be present in vertebrobasilar TIA or CVA
Weakness
Assoc with, gen/location, paralysis, onset, progression, mvmt affected?
TIA/CVA- wkns/paralysis
Focal wkns- ischemia, vasc, mass lesion CNS, PNS, MS DO, muscle diseases
Bilat prox wkns- myopathy
Myasthenia Gravis
wkns made worse by repeated effort and imp with rest
Loss of Sensation
numb, diff moving a limb, alter sens, tingling/pins-needles
Parasthesia
Limb goes to sleep= compresion of nerve, tingly. prickly, feeling of warmth, coolness or pressure.
If in hands and around mouth- hyperventilation
Dysesthesia
distorted sensation in repsonse to stim, may last longer than stimulus
Pain
May arise from neurologic causes but often reported with Sx of other body systems
Burning pain- painful sensory neuropathy
LOC/ fainting
Complete black out or hear voices.
Symptoms of feeling faint- light headed, weak, wo actual LOC- near/presyncopal
Anyone witness- Sz mvmt, onset/offset sudden/slow
Syncope
sudden temp LOC and postural tone- dec blood flow to brain
Cardiac- arrythmias cause- more common in older pt, sudden onset/offset. AS, HOCM, MI, Massive PE
Other causes of syncope: Hypocapnea d/t hyperventilation, hypoglycemia, hysterical fainting.
Unlike Sz- no incontinence, tonic-clonic mvmt, postictal state but may have bitten tongue or bruised limbs.
Vasovagal
young people with stress- warning symptoms- flushed, warmth, N- slow onset, slow offset
Seizures
Paroxysmal DO sudden excessive electrical DC in cerebral cortex or underlying structure. May or may not LOC. Any abn feelings, thought process, sensation, smells, abn mvmt.
Tremors
unable to controll trembling/shaking/body mvmt.
RLS
develops at rest, accompanied by urge to move, relief with walking. Usually occurs at night. CNS iron/dopamine def, or dysmetabolism. Chronic ext tissue pathology/inflammation
Tx: daily exercise, adequate sleep, Dopaminergic meds (Requip,Mirapex), Correction of Fe def.
Health Promotion
Stroke/TIA prevention
Reduced periphearl neuropathy
Three D’s
Stroke stats
Ischemia 80-85%
Hemmorhage 15-20%
ICH 10-15%
SAH 5%
TIA
sudden focal neuro deficit lasts less than 24 hours. Precursor to stroke, 3 months after TIA, 15% progrss to CVA esp if RF present.
Stroke warning signs
sudden numbness, wkns, confusion, aphasia/dysathria, understanding, walking, dizzy, loss of balance/coordination, trouble seeing in 1 or 2 eyes, severe HA
S/S of stroke depend on area affected
Most common MCA- visual field cuts, contralat hemoparesis, sens deficits
Left hemi-aphasia
Right hemi- neglect/inattention to opposite side of body
Stroke RF Primary prevention
modifiable RF- HTN, smoking, HPL, DM, obesity, lack of exercise, heavy ETOH. Careful mngmt afib, asymp carotid disease. For ICH/SAH- BP MNGMT. RF for SAH- smoking, HTN, ETOH abuse, family HX first degree relative
Stroke RF Secondary Prevention
If TIA, focus on cause: atherosclerotic lg vessel disease, carotid emboli, small vessel lacunar disease, idiopathic.
Younger pt- consider Takayasu arteritis, art dissection, fibromuscular dysplasia, cocaine, drug use. May need ASA/coumadin for prevention.
Peripheral Nueropathy
Polyneuropathy
Autonomic Dysfunction
Mononeuritis Multiplex
Diabetic Amyotrophy
Dementia
Alzheimers
Vascular
Lewy Body- Parkinsons
Frontotemporal
Depression neurotransmitters
Serotonin- if depleted: irratabilty, hostility, SI
Norepi depletion: dullness, lethargy
CN 1: Olfactory
Test for common odors one side at a time with eyes closed.
Loss of smell with: sinus conditions, head trauma, smoking, aging, cocaine, Parkinsons
CN 2: Optic
Inspect optic fundi, check disc. Test visual fields by confrontation bilaterally
Visual field deficits. Can occur with glaucoma, retinal hemm, optic neuritis. Bitemp hemianopsias-defect at optic chiasm- usually pituitary tumor.
Homonymous hemianopsias or quad in postchiasmal lesions- usually parietal lobe assoc w/CVA
CN 2&3: Optic and Oculomotor
Inspect size/shape pupil, can be 0.4mm between pupils.
CN 3 palsy- larger pupil abn constriction- parasympathetic denervation, ptosis, opthalmoplegia. In Horner’s Syndrome- pupils constrict to loght but d/t sym degen the affected pupil remains small(miosis) d/t abn pupillary dilator muscle
CN 3,4,6: Oculomotor, Trochlear, Abducens
EOM’s, ?diplopia, convergence, ?nystagmus, Look at distant object- check for inc/dec nystagmus, ?ptosis
Dysconjugate gaze?
Diplopia? Monocular with glasses/contacts/cataracts/astigmatism/ptosis. Binocular with CN 3/4/6 neuropathy (40%), muscle disease from MG/trauma/throid opthalmopathy, internuclear opthalmoplegia.
Nystagmus
cerebellar disease esp with gait ataxia & dysarthria & vestibular DO.
Ptosis
CN 3 palsy, Horner’s syndrome(ptosis, meiosis, anhidrosis), MG
CN 5: Trigeminal
M: Temporal & Masseter muscle
S: Pain at forehead, cheek & jaw, sharp vs dull. If abn- test for temp too. Also check for light touch.
Masseter- diff chewing
Pterygoid- diffmoving in opposite direction
Unilateral wkns- CN 5- pontine lesion
Bil wknsin cerebral hemispheris disease because of bil cortical innervation.
Corneal refelx: look away and touch cornea with something soft- should blink
Stroke pattern
facial/body sensory loss on same side but contralateral cortical or thalmic lesion.
Ipslateral face but contralateral body sensory loss in brainstem lesions
Trigeminal Neuralgia
isolated facial sensory loss in peripheral nerve DO
Absent corneal reflex
CN 5 or 7 lesion. Abs blinking and sensorineural hearing loss= acoustic neuroma
CN 7: Facial
raise eyebrows, frown, close eyes tightly, show upper and lower teeth, smile, puff out cheeks.
flattening of asolabial fold/drooping of lower eyelid- facial weakness
In unilateral paralysis, mouth droops on the paralyzed side when pt smiles or grimaces.
Bell’s Palsy
Injury to CN 7, affects upper and lower face, a central lesion affects lower face. Other symptoms Bell’s Palsy- loss taste, hyperacusis, inc or dec tearing
CN 8: Acoustic
Whispered voice; conductive vs sensorineural
AC/BC- Weber test
Rinne test
Hearing loss from: excess cerumen, otosclerosis, OM- hearing loss, presbyacusis- aging- usually SN loss
CN 9&10: Glossopharyneal & Vagus
Diff swallowing
mvmt soft palate and uvula when saying “AHHHH”
Gag refex
Hoarse = vocal cord paralysis
Nasal= palate paralysis
Check for unilateral palate mvmt= lesion CN 9 or CN10
CN 11: Spinal Accessory
shoulder shrug, turn head into hand on face
trapezius wkns with atrophy and fasiculations in PN DO. If paralysis- shoulder droops down and lat.
CN 12: Hypoglossal
tongue protruded, move side to side
Unilateral cortical lesion- tongue deviates away from side of lesion, toward side of wkns
Dysrthria and amyotrophic lat scleoris, polio
Hypertrophy or Pseudohypertrophy
check muscl bulk/atrophy/hypertrophy. Flattening in prominences between metacarpals suggests atrophy but in median and ulnar nerve damage.
Muscular Atrophy
PN DO- spinal cord, RA, protein calorie malnutrition
Dec Muscle Tone
PN DO, cerebellar disease or acute stages of spinal cord injury
Hypotonia
flaccidity, PN DO.
Paresis
wekness. Hemiparesis is one sided
Paralysis
plegia or absense of strength. Para- legs, Quad- all ext.
Weak grip
cervical radiculopathy, deQuervains tenosynovitis, carpal tunnel syndome, arthrits, epicondylitis
Wkns extention at elbow
radial nerve damage
Weak finger abduction
ulnar nerve DO
Weak opposition of thumb
median nerve DO- carpal tunnel
Myopathy
Proximal symmetric muscle weakness- muscle DO
Polyneuropathy
Distal symmetric muscle weakness- PN DO
Coordination= Cerebellum
RAS
Pt to Pt mvmt
Gait
Stand specified way
Coordination worsens with eyes closed
Dydiadochokinesis
cerebellar dysfunction. Cannot perform RAS- irregular and clumsy
Upper motor neuron wkns and basal ganglia disease may impair RAS but not same way
Dysmetria
While doing RAS, patient overshoots but corrects self and reaches goal.
Intention tremor
at the end of movement
Past pointing
Repetitve consistent deviation to one side, while eyes closed suggests cerebellar or vestibular disease
Ataxia
gait instability
causes: cerebellar disease, ETOH, loss of position sense.
Gait
across room, heel to toe, on heels, on toes, hop in one leg in place, shallow knee bend, rise from sitting
UA heels and toes- distal muscular weakness
UA heel walk- corticospinal tract damage
UA hop- wkns, lack of position snese, cerebellar dysfunction
UA shallow knee bend- prox muscle wkns
UA rising from sit- prox muscle wkns
Stance
Rhomberg
Pronator drift
Rhomberg
Position sense test- feet together, stand with eyes closed 30-60 seconds, min sway normal. Positive test= cerebellar ataxia
Pronator drift
Stand 20-30 sec arms forward palms up, eyes closed. Should be able to hold, tap down on arms, should be able to hold. Sens and Spec for corticospinal tract lesion
Downward drift with flex fingers and elbow may occur
Sideward/upward- loss position sense
Anestesia
abs of touch sensation
Hypesthesia
dec sensitivity
Hyperestesia
ins sensitivity
Vibration
1st sense lost in PN neuropathy. Common causes: DM, ETOH, Post colum disease- tertiary syphyllis or vit B def
Can use to test cord lesion on trunk
Astereoognosis
UA to recognize objects in hand with eyes closed
Discriminative Sensations
Stereognosis Graphestesia 2 Pt discrim Pt localization Extinction Alterations indicate lesion in sensory cortex
Hyperreflexia
CNS lesion along desc corticospinal tract
Look for assoc upper neuron- wkns, spasticity, + Babinski
Hyporeflexia
Diseases of spinal nerve root, Spinal nerve, plexuses, PN. Look for assoc lower motor unit disease- wkns, atrophy, fasciculations
Use reinforcement if dim or absent- isometric contraction of other muscle for 10sec before testing to inc reflex activity
Positive Babinski/Plantar Reflex
DF big toe, CNS lesion. Also from drug, ETOH, postictal after Sz
Meningeal Signs: Brudzinski
hands behind head while supine, flex neck forward, Normal neck supple. Stiff/Resistance in 90% with meningitis, 20-85% for SAH, also present in arthritis and neck injury
Meningeal Sign: Kernig
supine, flex leg at hip and knee, then straighten knee- may cause some discomfort but not pain. Pain is positive finding- If bilateral = meningeal irritation
Lumbosacral RadiculopathY
straight leg raise, DF foot, pain= + finding
Compression spinal nerve root as it exits vertebral foramen, assoc with wkns, dermatomal sensory loss, usually herniated disc, Most common herniated disc- L5-S1, spinal angles sharply. Ipsilateral calf wasting, wk ankle DF.
Sciatica
S1 distribution- low back pain with nerve pain that radiates down leg
Asterixis
ID metabolic encephalopathy when mental function impaired. Stop sign with hands, watch 1-2 minutes
Sudden breif nonrythmic flexion of hands/fingers: liver disease, uremia, hpercapnia
Winging of Scapula
Shoulder muscles weak or atrophic, push hands against wall- scapula lie close to thorax.
In winging, medial border of scapula juts backwards- wkns serratus muscle- MD or injury to long thoracic nerve
If thin, may appear winged
Stupous/Comatose Patient
ABC’s, LOC, Neuro exam
2 Don’t with coma pt
don’t dialate pupils- single most important clue about cause(structural vs metabolic)
Don’t flx neck if trauma
5 clinical signs strongly predict death
abs corneal reflex abs pupillary response abs WD to pain no motor response at 72 hrs, no motor response
Doll’s eyes
In comatose pt with no neck injury turn head side to side. Eyes should move toward opposite side. If eyes don’t move=midbrain or pons lesion
Oculovestibular Reflex with Caloric Stimulation
If oculocephalic reflex abs, assess brainstem fxn, not performed on an awake pt.Ice cold water into ear canal. If brainstem intact eyes will move toward cold water. No response= brainstem injury
CSF/Blood in nose/ears
suggests skull fracture or OM- possible brain absess
ACA
contralat leg wkns
MCA
largest vasc bed for stroke.
contralat facial, arm>leg wkns, sensory loss, field cut, aphasia(L MCA), or neglect,apraxia(R MCA)
Subcortical
contralat motor or sensory deficit w/o cortical signs
PCA
contralat field cut
cortical bindness, but pupil response present.
Brainstem/Vertebral or Basilar Artery branches
dysphagia, dysarthria, tongue/palate dev, ataxia, crossed sensory/motor deficits(ips face with contra s/m deficits)
Basilar Artery
Oculomotor deficits, ataxia, crossed s/m deficits
Complete occlusion= lock in syndrome
Tremors
Resting/Static
Postural/Action
Intention
Types of seizures
Partial: Simple partial, Complex partial
Gen: Grand Mal, Absence, Atonic or drop attack, Myoclonic
Pseudoseizures
Wernicke’s Aphasia
fluent receptive aphasia
Post superios temporal lobe
Broca’s Aphasia
non fluent expressive aphasia
Post inferior frontal lobe
Muscle Tone Disorders
spasticity
rigidity
flaccidity
paratonia
Speech Disorders
Aphonia
dysphonia
dysarthria
aphasia: exp/rec
Facial Dyskinesias
Tic Chorea Athetosis Dystonia Spatic Torticollis
