Ataxic, hyper, hypo, mixed
Clinical signs of cerebellar damage
Ataxia: incoordinated, clumsy, high fall risk
Dysmetria: X stop mvm, mvt under or overshoot
Dyssnergia: decomposition of mvm (errors in timing, speed)
Hypotonia
Asthenia: muscle easily tired
Tremor: intention tremor only seen during mvm, OK at rest
Disturbance of posture, gait (incoordination, loss of balance=falls)
Rebound phenomenon (neurologists ask pts to put hands out, tap on arm): exaggerated reflex of mvm, positive rebound means that they have cerebellum damage, possibly have ataxic dysarthria
Nystagmnus-involuntary eye mvms, eye will dart around
Ataxic dysarthria
Causes of cerebellar damage
Trauma
Vascular disease
Infections
Tumours
Toxic, metabolic, endocrine disorders
Demyelinating, hereditary
Extra-pyramidal system disorders
Extra-pyramidal system-multi-synaptic pathways indirectly connecting motor areas of cerebral cortex with LMN
Major components: basal ganglia, substantia nigra, red nuclei, subthalamic nuclei
Controls muscle tone for maintenance of posture, for supporting mvms
Pyramidal
Straight from motor cortex to LMN
Clinical signs
Hypokinesia
Hyperkinesia
slowness, poverty spontaneous mvm
Types: akinesia- X mvm at all, most disabling symptom
Characteristics: slowness in intiation, execution of vol mvms, slow shuffling gait-dev festinating gait
Bradykinesia
Affects speed that muscles are activated
Slow mvm, delayed or false starts-reattempt a mvm multiple times
Slowness once mvt begun, may be difficult to stop
Intermittent freezing/immobility
Loss of postural reflex, stooped look-rounding of shoulders, loss of muscular contraction to support body-core strength impacted.
Tremor at rest: most evident at rest (limbs, head), pill rolling- thumb-fingers rubbing tgt
Rigidity: increased muscle tone, slowness of mvt, feeling of stiffness, cogwheel rigidity
Aetiology
Parkinson's disease as most freq cause. Hypokinetic dysarthria occurs in approx 70-90% of all cases. Increase in prevalence, severity as disease progresses. Degeneration nerve cells, also possible if someone has vascular lesion in extra pyramidal systemtracts in corpus striatum, substantia nigra-deficiency of neurotransmitter dopamine
Any process that damages extrapyramidal system-stroke, cerebral hypoxia, TBI, toxic-metabolic conditions (neuroleptic, anti-emetic drugs)
abnormal excessive involuntary mvm
2 Types
Quick
Slow
Myoclonic jerks: abrupt, sudden, unsustained, irregular, muscles of limbs, face, oral cavity, soft palate, larynx, diaphragm-affects speech
Tics: Brief, unsustained, recurrent, compulsive moments of small part of body eg. Tourette syndrome with multiple tics, uncontrolled vocalisations (grunting, coughing, barking), coprolalia (involuntary swearing)
Chorea: single, unsustained, muscle action --> short, rapid, uncoordinated jerks of trunk, limb, face, tongue or diaphragm, irregular, unpredictable patterns. 2 major diseases: Huntington's chorea, Syndenham's chorea
Ballismus (hemiballismus): wild flailing mvms on one side of body, marked in arm, facial muscle
Athetosis
Dyskinesia
Dystonia
Huntington's chorea
What is it: chronic degenerative neurological disorder, progressive chorea, intellectual deterioration, decreased cognitive functioning.
Inherited condition: begins in adult life, fatal 10-20y post onset.
Lesions: loss of neurons w/i caudate nucleus, putamen, cerebral cortex, white matter
Features: facial grimacing, head jerks, weaving mvm of arms and shoulders, twists, jerks of body, increased muscle tone, problems w coordination
Continuous, arrythmic, slow writhing-type mvms
Irregular respiratory cycling: unable to regularly inhale, exhale. Decreased vital capacity, difficulty controlling prolonged exhalation, laryngeal spasm, incoodination of phonation, articulation, monopitch, artic errors
Lingual, facial, buccal, peri-oral areas
Repetitive, slow, writhing, flexing, extending voluntary mvm with tremor
Tardive dyskinesia, levodopa-induced kinesia (effect of dopamine medications to replenish dopamine BUT this medication then causes excessive involuntary mvm)
Slow, sustained for prolonged periods
Speech muscles-facial spasms, prolonged lip pursing, invl twisting, protrusion of tongue
Essential tremors
Tremors-involuntary mvms resulting from contraction of opposing muscle groups
Absent at rest-appears when muscles act to move or support body part
Slowly progressive-hands, heads commonly affected
May affect laryngeal muscles-organic voice tremor-excess low pitch, monopitch, strained, strangled quality, pitch breaks, harsh
Mixed dysarthria
What is it?
3 neurological conditions
1 level of nervous system damaged
Aetiology: CVA, TBI (most common), inflammatory disease, degenerative conditions
ALS
Multiple sclerosis
TBI
What is it: form of MND, selective, progressive degeneration of corticospinal, corticobulbar pathways, severe weakness of bulbar musculature, both UMN, LMN lesions , dev b/w 60-70 y/o, die usually 1-5 years from onset
Aetiology: variety of hereditary, traumatic, toxic, viral, but mostly unknown
Problems: swallowing, aspiration, saliva control, speech
Types of dysarthrias: Flaccid-spastic dysarthria. BUT overall: more spastic > flaccid. Flaccid-phon and reson, spastic-prosodic excess, insufficiency, artic, reson incompetence, phon stenosis (at lvl of VF)
What is it: most common demyelinating disease, is a major cause of neurological disability in young adults (peak onset 20-40y/o females slightly more affected than males),
Caseload: 2/3 cases periods where symptom get worse, remission (period of hiatus where things return to near normal), 1/3 cases progressive without remission. Majority: significant disability wrt motor, cognitive function
Aetiology: unknown-metabolic, immunological, inflammatory, viral. Most common in temperate climates. Lesions- white matter CNS-demyelination causes scarring (sclerosis) of brain tissue- seen as plaques in white matter, may affect a number of diff parts in CNS
Symptoms: optic neuritis, motor difficulties, incontinence, dysarthria, dysphagia, seizures, mood affected, cognitive and memory problems
Dysarthria-Approx 1/3 problems with commn in TBI Population. Wide range of severity-can be from mild artic imprecision to total unintelligibility. Long term outcome-persistent disorder
Aetiology: falls, MVAs
Prognosis: poor BUT functional speech has been recovered long after acceptable period of neurological recovery