Clinical Flashcards
What is the main function of the cerebellum?
Coordination of the motor systems to all precision motor movements and accurate timing of precision motor movements.
Where are the cerebellar afferents and efferent fibres from?
Afferent
spinal cord (spinocerbellar fibres)
Inferior olivary complex - olivocerebellar fibres
Vestibular system - vestibulocerebellar fibres
Pontocerebellar fibres from the cerebrum via the pontine
Efferents to:
Lateral vestibular nuclei, red nucleus and reticular formation
What is ataxia?
Uncoordinated movements
What are the symptoms of cerebellar disease?
Ataxia - speech/swallowing difficulties, limb clumsiness (falls common), torso (difficulty sitting), gait (wide stance)
Dysarthria (slurred speech), dysphagia (difficulty swallowing).
May also have visual symptoms (oscillopsia/diplopia), vertigo (sensation of movement), nausea and vomiting.
What is dysarthria?
Slurred speech
What is dysphagia?
Difficulty swallowing.
What are the signs of cerebellar disease?
Abnormal eye movements: nystagmus, square wave jerks.
Dysarthria - laboured/slurred, staccato (broken sounds), rapid tongue movements slowed.
Limb ataxia - intention tremor, past pointing (dysmetria), impaired rapid alternating movements
Truncal and gait ataxia - may be the only sign, broard based gait, sways, irregular steps in time/distance.
What is dysmetria?
Over or undershoot for objects when pointing or grasping.
What happens to tone, reflexes and sensation in cerebellar disease.
There is no muscle weakness
Tone - normal to decreased
Reflexes - normal
Sensation - normal
What are some of the causes of cerebellar disease?
Toxins - alcohol Congenital abnormalities Strokes Inflammation/demyelination Tumours Infections Degenerative disorders
What are some reflexes and their nerves/spinal levels?
Jaw reflex - trigeminal nerve Biceps - C5 Brachioradialis -C6 Triceps C7 Fingers - C8 Knee - L3/L4 Ankle -S1
What is tone?
The resistance of muscles to passive lengthening. It requires muscle elasticity and neural input.
What happens to muscles in peripheral motor neuron lesions?
Tone - decreased Muscle wasting Reflexes - decreased/absent Muscle fasciculations Flexor plantar response Normal rapid alternating movements. Power is reduced
This involves diseases of snesnory axons, cell bodor of motor neuron or axon of motor neuron.
What happens to muscles in upper motor neuron lesions?
Reflexes - increased (spasticity) Tone - increased Plantor - extensor Power - reduced Rapid alternating movements - reduced
Seen in strokes, brain tumours, spinal cord lesions
What happens to muscles with a spinal cord lesion at C5?
Bicep and supinator jerks - reflexes decreased, tone at elbow is decreased.
For lower myotomes the reflexes are increased (tricep - C7, fingers C8, knee L3, and ankle S1)
Tone in the lower limbs is increased.
What are the motor symptoms of parkinson’s disease?
Rest tremor - pill rolling tremor - tremor is lost with posture
Bradykinesia - slow movement, emotionless face, impaired rapid alternating movements, reduced or absent arm swinging, shortened stride length, freezing, decrement (starts fast but movements slow until stopped an has to start over)
Rigidity - cog wheel
Postural instability and gait abnormalities - difficulty standing from a chair, rolling over, stooped/flexed position, tendency to take several steps to turn, falls
What are the non-motor symptoms of parkinsons disease?
Depression, anxiety, dementia, anosmia (loss of smell), constipation, pain, sleep disturbances, change in mood, ANS dysfnction
What is the Braak staging system for parkinson’s disease?
Stage 1: vagus nerve and olfactory nerve
Constipation and sense of smell reduced
Stage 2: Reticular formation - REM sleep disturbance
Stage 3: substantia nigra - physical symptoms
Stage 4: Temporal cortex - memory problems
Stage 5: Neocortex and prefrontal cortex - dementia
What are the pathogenesis of parkinson’s disease
degredation of the dopamine neurons in the pars compacta f the substantia nigra.
Accumulation of Lewy bodies in those damaged neurons containing alpha synuclean
There is a genetic component alpha synuclean gene
Toxins can cause it rapidly - MPTP parkinsonism
Infection
How is OD diagnosed?
Two cardinal signs - resting tremor, bradykineia, rigidity, postural anormalities
Progressive course
Response to levodopa
No other cause
What are the treatments for parkinson’s disease?
Levodopa + dopa decarboxylase inhibitor (carbidopa)
Anticholinesterases
Monoamine oxidase B inhibitor
Apomorphine: Liquid absorbed from subcutaneous fat avoiding first pass metabolism
Duodopa: Liquid levodopa absorbed from the duodenum to get around short half life
Stereotactic thalamotomy (for tremor) Stereotactic pallidotomy (improve all features of Parkinson’s disease, including dyskinesias) Transplantation of dopamine-producing tissue (e.g. fetal tissue) Deep brain stimulation (inhibits overactive neurons without the need for a destructive procedure)
