Neuro WK 1: Basics

Dysdiadochokinesia

________= impaired ability to perfrom rapid alt mvmt, mvmt are irregular w /rapid loss of range and rhythm as speed increases.

Somatognosis

________: difficulties in reference points to the outside world; contralateral side, distinguishing their extremity from therapists extremitiy.

Multiple sys atrophy

________ (shy- drager syndrome): rare and progressive deterioration of cerebellar, BG, and brainstem.

Dysmetria

________= unable to control range of mvmt (hypo or hyper)

Cognition

________= process of knowing (awareness & judgement)

Coordination deficits

________ transfers: worse in stand, unsafe foot placement and arm reaching, poor balance reactions.

CG

Bradykinesia bed mobility: inc time to complete leads to fatigue and ________ burnout.

Dyskinesia

________= invol, erratic, writhing mvmt of face, arms, legs, or trunk.

non verbal

Late stage HD: ________ /completely unintelligible, in W /C or bed, transfers difficult, chorea severe, increase rigidity and contractures, cognitive symptoms increase.

Reactions

________: automatic overflow response, in response to effort; obligatory and not controlled.

Progressive supranuclear

________ palsy: neuron degneration in many parts of the brain- BG & brainstem.

Spinocerebellar ataxia

________: involves BG, cerebellum, and sensorimotor cortex.

Athetosis

________= continuous stream slow, flowing, writhing invol mvmt.

Paresis

________= weakness, partial loss of vol contraction.

Graphesthesia

________= traced figure identification.

Myoclonus

________ causes: liver /kidney failure, TBI, metabolic disorders (high /low blood sugar, low Ca, Mg, or Na), alzheimers, creutzfeldt- jakob disease, seizure disorders.

Goals of Neuro Rehab

Help pt establish realistic goals and understand/manage condition, capitalize on strengths, prevent/minimize/eliminate impairments, minimize/eliminate enviornmental barriers, improve QoL, assist family/CG

Neuro eval components

review medical hx, sys review, subjective info (pt, family, CG), mottor assessment, sensory assessment, spatial/visual assessment, respiratory assessment, cognitive/communication assessment, ADL, functional assessment

Core outcome measures

berg balance, functional gait, activities specific balance confidence, 10 meter walk, 6 min walk, 5x STS

Disorders of speech

Apashia, Dysarthria, Dysphonia

Cardiopulm Screen (normative values)

HR= 60-90, BP=120/80, RR= 12-20

UMN signs

weakness, spasticity, increased reflexes, clonus, Babinski, muscle bulk preserved

LMN sign

weakness, hypotonia, decreased reflexes, fasiculations, early atrophy

UMN syndrome

+ signs= spasticity, stereotyped mvmt synergies, spasms, Babinski + clonus exaggerated DTRs

UMN syndromes

signs= paresis/paralysis, loss of dexterity, fatigue

Spasticity

velocity-dependent increase in resistance to passive stretch

Spasticity UE

SH ADD and IR, elbow flexors, wrist & finger flexors, forearm pronators

Spasiticy LE

hip ext, IR, ADD, knee extensors, ankle PF

Spasticity influenced by

effort, stress, body position, meds, enviornment, arousal, alertness, time, joint ROM, injuries, age, and chronicity of disease

Penn Spasm Scale Frequency

0= no spasm, 1= mild via stim, 2= infrequent full 1/hr, 3= more than 1/hr, 4= more than 10/hr

Penn Spasm Scale Severity

1= mild, 2= mod, 3= severe

Rigidity

increased resistance to passive stretch that is IND of velocity; uniform in both directions

Measure Rigidity

0= none, 1= slight/detectable, 2= mild-mod, 3= marked full ROM easy, 4= marked full ROM difficult

Decorticate

UE flex & LE ext

DEcErEbrateE

UE & LE ext

Opisthotonus

strong sustained contraction of neck and trunk extensors

Reactions

automatic overflow response, in response to effort; obligatory and not controlled

Primitive Reflexes

ATNR, STNR, Tonic Labrynthine

Common paralysis

hemiplegia, paraplegia, tetraplegia, and monoplegia

CANNOT accurately assess MMT grade

do not have isolated muscle contractions, demonstarte synergistic mvmt, sig abnormal muscle tone, connot follow instructions

Fractionation

the ability to move a single jt w/o simultaneously producing unnecessary mvmt in other jts

Atrophy

loss of muscle bulk

Disuse atrophy

loss of muscle bulk d/t lack of use

Neurogenic atrophy

loss of muscle bulk d/t damage to NS

LMN

atrophy early

UMN

atrophy later

Muscle spasm

invol muscle contraction

Cramps

severe, painful spasm

Fasiculations

quick twitches of muscle fibers of a single motor unit that is VISIBLE on the surface

Fibrillations

(LMN lesion) breif contraction of a single muscle fiber NOT VISIBLE on the surface

Two-pt discrimination

sense difference in contact points

Somatognosis

difficulties in reference points to the outside world; contralateral side, distinguishing their extremity from therapists extremitiy

Anosognosia

pt does not recognize their impairments or functional limitations

Goals

impairments ALWAYS have to measurable AND linked to a functional activity

UMN motor cortex or connections btw brain and SC

exaggerated reflexes, decreased motor selection, spasticity, mvmt synergies, early flaccidity, and weakness

UMN basal ganglia

invol or decreased mvmt, decreased mvmt pattern flexibility

UMN cerebellum

loss of coordination

Parkinson Hallmark signs

rigidity (neck), akenesia/bradykinesia (UE), facial masking, speech defecits (low, rapid, dysarthria), resting tremor

Parkinsonism/Atypical parkinson/parkinson-plus

does not respond to dopaminergic meds, bradykinesia w/ degradation of repetitive mvmt, not just basal ganglia

Dx Parkinson Plus

Multiple sys atrophy, corticobasal degeneration, drug-related, infectious, toxic, structural

Vascular parkinsonism (arteriosclerotic pseudoparkinsonism)

LE emphasia w/ gait and cognitive impairments

Chorea

invol, rapid, irregular, and jerky mvmt involving many jts

Chorea causes & symptoms

dysregulation of basal ganglia motor circuit; excess dopamine (thalamo-cortical output increased)

Causes of Chorea

huntington disease, pregnancy, benign hereditary chorea, infection/immune related (sydenhams chorea), systemic lupus erythematosus, focal vascular lesion BG, drugs (levodopa, neuropletics, and oral contraception), metabolic disorders (hyperthyroidism, hypo/hyper-parathyroidism and hypo/hyper-glycemia)

Challeneges Chorea

increase anxiety and vol mvmt, subsides during sleep, abnormal mvmt, athtosis (writhing mvmt)

Treatment Chorea

depends on etiology, meds (neuroleptic, dopamine depleters, and benzodiazepines)

Huntington Disease

hereditary, neurodegenerative, gene on 4th chromosome

S&S HD

chorea, dystonia, falls

Juvenile HD

rare, symptoms begin

Middle stage HD

need AD to ambulate, no longer able to drive, work, IADL, basic ADL difficult, difficulty w/ speech and swallowing, chorea mvmt more prominent (skilled vol mvmt difficult, cognitive changes worsen)

Late stage HD

non-verbal/completely unintelligible, in W/C or bed, transfers difficult, chorea severe, increase rigidity and contractures, cognitive symptoms increase

Medical treatment HD

tetrabenazine, haloperidol, fluphenazine, seizure meds, depression meds

HD rehab

PT, OT, PT, psych & social worker, homecare/long term/hospice

PT early

pt ed, general strength, ROM, aerobic training

PT middle

balance, AD, home safety set up

PT late

family/CG ed, safety and comfort measures, positioning, massage, PROM, QoL measures

Ataxia potential causes

TBI, abnormal nutrition, mitochonrial disease, autoimmune syndromes, friedrich ataxia

Ataxia characteristics

dyscoordination UE/LE, wide BoS, irregular speech/swallowing

Progressive ataxia

spinal cord, peripheral nerve, cerebellum degenrate

Progressive ataxia S&S

UE mvmt uncoordination, speech slurred, congenital clubfoot/scoliosis, changes w/ vibration/position sense, decrease mental fx, slight tremor, heart problems

Spinocerebellar ataxia

progressive atrophy of cerebellum; symptoms vary

Spinocerebellar ataxia challeneges

sensation, muscle weakness/stiffness, RLS, tremors, dystonia (twitching of face & tongue, eye bulging), loss of coordination & balance, speech & eye mvmt

Spinocerebellar ataxia

mixed involvement general dystonia, dystonic posturing

Spinocerebellar ataxia

involves BG, cerebellum, and sensorimotor cortex

Spinocerebellar ataxia

initiated/worsened by vol action and associated w/ overflow muscle activation

Spinocerebellar child

progress to general dystonia

Spinocerebellar ataxia adult

remains focal

Spastic dystonia

post stroke or ABI

PSP

vertical gaze paralysis (hallmark), surprised/frightened expression, rigidity & bradykinesia, speaking/swallowing, insomina, emotional dysregulation

PSP early stage

sig impulsivity

PSP late stage

depression and dementia, sig mvmt disabilities

Multiple sys atrophy (shy-drager syndrome)

rare and progressive deterioration of cerebellar, BG, and brainstem

MSA Parkinsonian type S&S

rigid muscles, bradykinesia, tremors, impaired posture & balance

MSA Cerebellar S&S

imparied mvmt/coord, unstead gait & LOB, slurred/slow/low volume speech (dysarthria), visual disturbances/blurred or double vision, dysphagia, orthostatic hypotension, high BP supine, irregular HR, dcreased sweating, sleeping disorders

PT MSA

maintain mobility, reduce contractured, and decrease muscle spasms and abnormal posture

Tremor & essential tremor

unintentional, rhythmic oscillation of body part in a fixed plane, contractions of agonist & antagonist muscles in sagittal pattern, resting tremor in body part not activated and completely supported against gravity

Action tremor

occurs w/ vol muscle contraction

Essential tremor

postural & action tremor, begin early, increase severity over time, exacerbated by stress, exercise, fatigue, caffine, meds, improves w/ relaxation and alcohol

Myoclonus

high speed contractions muscle/group of muscles

Myoclonus causes

liver/kidney failure, TBI, metabolic disorders (high/low blood sugar, low Ca, Mg, or Na), alzheimers, creutzfeldt-jakob disease, seizure disorders