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MBBS IV - Junior Clerkship WCS > JC23 (Medicine) - Cerebellar Lesions and Gait Disorders > Flashcards

JC23 (Medicine) - Cerebellar Lesions and Gait Disorders Flashcards

1
Q

Outline the anatomical components to control normal gait

A

□ Higher control: premotor cortex, motor cortex >> Pyramidal tract

□ Pattern generator:

Midbrain locomotor region (MLR) generates drive

Spinal locomotor network (SLN) allows rhythm generation and pattern formation

>> Reticulospinal tract

□ Effector: spinal reflex pathways to PNS/ motor unit

□ Regulation: Extrapyramidal system → upper level (initiation) Cerebellar system → middle level (synergy) Spinal reflex pathways → lower level (effector)

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2
Q

Anatomical components that control initiation, pattern, rhythm and end of normal gait?

A

Initiation:

  • Premotor
  • Motor cortices

Synergy: subcortical centres

  • Mesencephalic/ Midbrain locomotor region (MLR)
  • Spinal locomotor network (SLN)
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3
Q

Anatomical components that control posture and balance of normal gait

A

Regulatory:

  • Basal ganglia
  • Cerebellum
  • Vestibular/proprioceptive apparatus
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4
Q

List 7 types of gait disorders

A

Ataxic gait

Parkinsonian gait

Hemiplegic/ diplegic/ spastic gait

Apraxic gait

Antalgic gait

LMN gait: Myopathic Waddling gait, Neuropathic steppage gait

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5
Q

Features of hemiplegic gait

A

unilateral arm + leg paralysis

Features: mimicks ancient reflexive gait

Arm: adducted and internally rotated at shoulder, flexed at elbow, pronation of forearm, flexion of wrist and fingers

Leg:

  • Abduction and circumduction at hip to prevent dragging
  • Knee extended, foot plantarflexed and inversion at foot
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6
Q

Features of paraplegic gait

A

spastic paraplegia

□ Features: scissor-like posture due to adductor spasm + extensor tightness

→ Strong adduction at hips

→ Two legs perform circumduction

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7
Q

Features of Parkinsonian gait

A

Features:

□ Flexed, stooping posture

□ Bradykinesia: hesitation in starting, freezing

□ Festination: initial hesitance

→ leans forward to initiate walking

→ hurries in shuffling steps to ‘catch-up’ on himself

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8
Q

Features of apraxic gait

A

Cause: bilateral frontal lobe or hemispheric diseases

Features:

□ Wide-based gait

□ Poor initiation – leg appear stuck to the floor

□ Tendency to fall backwards

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9
Q

Features of ataxic gait (cerebellar or sensory ataxia)

A

Cerebellar ataxia: ‘drunken’ gait

  • Wide-based (shoulder-wide) Jerk and unsure steps varying in size
  • Trunk sways forward
  • May only be detectable in tandem gait in mild cases

Sensory ataxia: ‘stomping’ gait

  • Gait appear normal with eyes open
  • Feet appear to ‘stomp’ on ground → to enhance proprioceptive input
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10
Q

Features of neuropathic gait

A

□ Cause: LMN weakness of pretibial and peroneal muscles (dorsiflexors)

□ Features:
→ Leg lifted high for toe clearance
→ Toes touch ground before heels

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11
Q

Features of myopathic gait

A

□ Cause: proximal myopathy → bilateral hip adductor weakness → inability to fix pelvis during walking

□ Features: ‘waddling gait’
→ Bilateral dropping of pelvis
→ Appears as swaying buttocks

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12
Q

Features of antalgic gait

A

□ Cause: pain with weight bearing
□ Feature:
→ Shortened stance relative to swing phase

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13
Q

7 types of hyperkinetic disorders

A

Chorea

Ballismus

Athetosis/ Choreoathetosis

Dystonia

Tremor

Myoclonus

Tics

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14
Q

Define tremor

A

alternating contractions of antagonistic muscle groups causing involuntary rhythmic oscillation of body parts

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15
Q

3 major types of tremor

A

□ Rest tremor: occurs in supported body parts w/o ms activation

□ Postural tremor: occurs when maintaining certain posture

□ Kinetic tremor: occurs during voluntary movement

→ Simple kinetic tremor

→ Intention tremor

→ Task-specific tremor e.g. writing

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16
Q

1 Example of rest tremor

Features

A

Parkinsonian tremor:

Coarse, low-frequency (3-4Hz) tremor

Typically starts at unilateral UL and spread to other limbs

Associated with rigidity and bradykinesia

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17
Q

2 examples of kinetic tremor

Features

A

Essential tremor

  • Variable amplitude, high-frequency (8-10Hz) tremor
  • Postural and kinetic tremor, NOT at rest
  • Typically affects bilateral arms (not LL) and head

Cerebellar tremor

  • Coarse, low-frequency (4-6Hz) tremor
  • Intention tremor
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18
Q

1 example of postural tremor

Features

A

Physiological tremor

Low-amplitude, high frequency (10-12Hz) tremor

Symmetrical and distal in distribution

Not evident in normal circumstances

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19
Q

Triggers of physiological tremor

A
  1. anxiety,
  2. emotional stress,
  3. drugs (eg. β2-agonist and other catecholaminergic drugs, lithium, antidepressants),
  4. alcohol/opioid withdrawal,
  5. thyrotoxicosis,
  6. fever
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20
Q

Describe chorea movement

A

sudden, unpredictable/ Random**

quasipurposive

involuntary fidgety/jerky movement

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21
Q

Describe Athetosis movement

A

slower, coarser, more writhing movement, esp affecting distal parts of limbs

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22
Q

Describe Ballism movement

A

involuntary movement that are proximal and large amplitude with a flinging/kicking character

□ Most often unilateral (hemiballism)
□ Classically a/w contralateral subthalamic nucleus stroke

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23
Q

Causes of choreiform movements

A

disruption in basal ganglia circuitry resulting in imbalance between indirect and direct pathways

□ Inherited: Huntington’s disease, Wilson’s disease, neuro-acanthocytosis…
□ Vascular: basal ganglia stroke
□ Inflammatory: Sydenham chorea, SLE, vasculitis
□ Neoplastic: Basal ganglia tumours, paraneoplastic chorea
□ Drugs: neuroleptics, levodopa, DA, antihistamines, amphetamines, digoxin, OC pills
□ Infectious: AIDS, neurosyphilis, cerebral malaria…
□ Metabolic: kernicterus, polycythaemia vera, hypoparathyroidism, chorea gravidorum (in pregnancy)

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24
Q

Diagnosis and management of choreiform movement disorders

A

Diagnosis: Hx, neurological/CVS exam + slit-lamp examination

Mx: tetrabenazine and clonazepam for symptomatic

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25
Q

Tics

  • Describe
  • Types
  • Control?
A

abrupt stereotyped repetitive movements involving discrete muscle groups

□ Can mimic normal coordinated movements, vary in intensity and lack rhythm
→ Motor tics, eg. eye-blinks, shoulder shrugs, facial grimaces…
→ Phonic tics, eg. barks, grunts, swearing…

□ May be temporarily inhibited by will power and usually disappear by sleep

26
Q

Causes of primary tics (-)

2 types of primary tics

A

no underlying structural lesions, usually onset in childhood and resolves after 20y

→ Transient tic disorder: last <1y, occurs in normal children
→ Gilles de la Tourette syndrome: otherwise unexplained motor + phonic tics with onset <21y

27
Q

Causes of secondary tics (-)

A

tics begin abruptly, are persistent or are problematic

→ Eg. dopaminergic drugs, stimulants, neuroleptics, other inherited diseases

28
Q

Management of tics (-)

A

Behavioural Tx (eg. habit reversal treatment) as mainstay

Drugs:

□ D2 blockers: haloperidol, pimozole, aripiprazole → risk of tardive dyskinesia → ↓use nowadays
□ Dopamine depleters: tetrabenazine → usually 1st choice nowadays after failure of behavioural Tx
□ α-agonists: guanfacine, clonidine → used if concomitant ADHD + Tourette syndrome

29
Q

Describe Myoclonus

A

brief, repetitive, involuntary sudden ‘shock-like’ jerks of muscle groups

Results from focal discharge from cortex (majority), subcortical or spinal cords

30
Q

Causes of myoclonus (-)

A

□ Physiological: hypnic (during sleep transitions), anxiety-related, exercise-related

□ Essential myoclonus

□ Epileptic myoclonus: a/w seizure syndrome, eg. juvenile myoclonic epilepsy

□ Symptomatic (secondary) myoclonus:
→ Focal CNS lesions, eg. post-stroke, CNS tumour
→ Metabolic and toxic encephalopathies
→ Neurodegenerative diseases, eg. CJD, Alzheimer’s disease, CBD
→ Metabolic storage diseases
→ Progressive myoclonic epilepsy (with progressive cognitive decline, seizures, ataxia and death)

31
Q

Describe Dystonia

A

Sustained/intermittent involuntary muscle contractions in antagonistic muscle groups causing abnormal movements or distorted postures

Dystonic movements are typically patterned, twisting and may be tremulous, i.e. dystonic tremor

32
Q

Types of Dystonia (-)

A

□ Focal: a group of muscles, eg. blepharospasm, oromandibular dystonia, cervical dystonia

□ Segmental: contiguous groups of muscles, eg. craniobrachial dystonia, Meige syndrome

□ Multifocal: ≥2 non-contiguous groups of muscles

□ Generalized, eg. idiopathic torsion dystonia

33
Q

Dystonia (-)

  • Exacerbating factors
  • Relieving factors
  • Extent of limb involvement
A

Exacerbating factors: voluntary action, fatigue, stress and emotional states

Relieving factors: sensory tricks (geste antagoniste, eg. touching face), sleep and relaxation

Extent of limb involvement: LL onset in early onset vs facial, neck or UL onset in late onset

34
Q

3 causes of dystonia (-)

A

Idiopathic torsion dystonia:

→ Hereditary: early onset (<21y), LL focal onset becoming generalized

→ Sporadic: adult onset (>21y), UL, facial or cervical onset w/o generalization

Secondary dystonia

→ Brain injury, eg. cerebral palsy, head injury
→ Neurodegenerative diseases, eg. Parkinsonism, spinocerebellar ataxia, Huntington’s disease
→ Drug-induced, eg. anticonvulsants, CCB, DA-agonist, levodopa, neuroleptics

35
Q

Treatment of dystonia (-)

A

Pharmacotherapy:

levodopa (if young-onset), anticholinergic/BZD (if adult-onset)

Botox injection

36
Q

3 Anatomical divisions of cerebellum

3 Functional divisions of cerebellum

A

Anatomical: Anterior lobe, Posterior lobe, Flocculonodular lobe

Functional:

  • Vestibulocerebellum - flocculonodular lobe for vestibular reflexes
  • Spinocerebellum - Vermis and intermediate zone for error-detection of truncal and distal muscles
  • Cerebrocerebellum - hemisphere for motor planning, rapidly alternating movement
37
Q

Clinical features of midline cerebellar lesion

A

Spinocerebellum - Vermis and intermediate zone for error-detection of truncal and distal muscles

□ Nystagmus: horizontal or vertical nystagmus
□ Truncal ataxia: wide-based cerebellar gait, Romberg –ve
□ LL dysmetria: heel-shin test

38
Q

Clinical features of hemispheric cerebellar lesions

A

Cerebrocerebellum - hemisphere for motor planning, rapidly alternating movement

abnormalities in limb coordination
□ Limb ataxia: UL dysmetria, intention tremor, dysdiadochokinesia, rebound, gait ataxia
□ Scanning dysarthria: same emphasis put on each syllable

39
Q

Acute causes of cerebellar signs

A

Vascular
 Cerebellar ischaemia
 Cerebellar haemorrhage

Drugs and toxins*
 Antiepileptics, eg. phenytoin
 Chemo, eg. cytarabine, 5FU
 Alcohol

Infectious
 Meningoencephalitis
 ADEM

40
Q

Subacute causes of cerebellar signs (-)

A

Autoimmune*
 Multiple sclerosis
 Miller-Fisher syndrome
 SLE, Behcet’s, coeliac…

Paraneoplastic degeneration*
 SCLC, gyne, breast, lymphoma

Neoplastic, esp CPA tumours

Metabolic*
 Chronic alcoholism
 Wernicke encephalopathy (vitamin B1 deficiency)
 Vitamin E deficiency
 Hypothyroidism

41
Q

Chronic progressive causes of cerebellar signs (-)

A

Congenital
 Chiari malformation
 Dandy-Walker syndrome
 Cerebellar agenesis

Hereditary*
 Spinocerebellar ataxia (AD) - SCA
 Friedreich’s ataxia (AR) - FA
 Ataxia-telangiectasia (AR) - AT
 Wilson’s disease (AR)
 Mitochondrial diseases

Neurodegenerative*
 Multiple system atrophy (MSA)
 Progressive supranuclear palsy (PSP)
 Cerebellar degeneration

42
Q

Define Parkinson’s disease

A

idiopathic degeneration of substantia nigra with intraneuronal Lewy bodies

43
Q

Classic symptoms of parkinonism

A

Extrapyramidal symptoms:

  1. Tremor: develops early unilaterally, 4-6Hz, decrease in late stage due to bradykinesia and rigidity
  2. Rigidity: ‘Cogwheel’ or ‘lead-pipe’ rigidity, flexed/stooped posture
  3. Akinesia or bradykinesia: slowness, hesitance, motor arrest
  4. Postural instability: imbalance and falls, propulsion/ retropulsion when standing
44
Q

Examples of bradykinesia due to Parkinson’s

A

Loss of finger dexterity

Shuffling gait

Masked face

Monotonous speech

Drooling saliva (slow swallowing)

45
Q

Ddx Parkinson’s disease

A

Idiopathic Parkinsonism (Parkinson’s disease, PD): commonest, 80% of cases

Parkinsonian-plus syndromes:
□ Multisystem atrophy (MSA)
□ Progressive supranuclear palsy (PSP, Steele-Richardson-Olzewski syndrome)
□ Corticobasal degeneration (CBD)

Secondary (symptomatic) parkinsonism:
□ Post-encephalitic, eg. encephalitis lethargica
□ Drug-induced, eg. dopamine-depleting/anti-dopaminergic drugs, lithium, antihistamines
□ Chronic head trauma, eg. ‘punch-drunk’ syndrome
□ Neoplastic, eg. parasagittal meningioma

Inherited neurodegenerative diseases:
□ Wilson’s disease
□ Hallervorden-Spatz syndrome

Pseudoparkinsonism:
□ Cerebral arteriosclerotic disease

Essential tremor, Cerebellar tremor (intention), Akinetic Huntington’s chorea

45
Q

Pathophysiology of Parkinson’s disease

A

□ Motor symptoms: Depletion of dopaminergic neurons, degeneration of nigrostriatal pathway → ↓dopamine input to striatum → balance shifted towards indirect pathway → bradykinesia, rigidity

□ Cognitive symptoms: degeneration of mesocortical/mesolimbic dopaminergic pathways

□ Autonomic dysfunction: dopamine depletion in hypothalamus

□ Dementia: degeneration of cholinergic nucleus (spread of Lewy Bodies to cortex)

46
Q

List non-motor symptoms of Parkinson’s disease

A

Neuropsychiatric:

  • Depression
  • Anxiety
  • PD-psychosis: common in late stages, can be due to levodopa

PD-Dementia

Autonomic dysfunction:

  • Postural hypotension
  • Constipation
  • Sweating

Miscellaneous: fatigue, pain, sleep disturbance, sexual disturbance, anosmia

47
Q

Severity staging of Parkinson’s Disease

A
48
Q

Clinical red flags of parkinsonism

A

Presentation:
* Young onset with strong family history
* Rapid progression
* Early instability and falls
* Early and prominent dementia

Extent:
* Pyramidal/ cerebellar signs
* Autonomic dysfunction

Treatment:
* Poor response to Levodopa

49
Q

Outline Clinical Diagnostic criteria of Parkinson’s disease ***

A

UKPD Society Brain Bank Clinical Diagnostic Criteria

Clinical features: Bradykinesia + at least one of:

  • Muscular rigidity,
  • 4-6Hz rest tremor,
  • postural instability without primary visual, vestibular, cerebellar or proprioceptive_dysfunction

Exclusion criteria: exclude other diseases

Supportive prospective positive criteria: 3+ for def. dx
Unilateral onset
Rest tremor present
Progressive, persistent asymmetrical involvement
excellent response to levodopa for 5 years or more
Severe levodopa induced chorea
clinical course of ten years or more

50
Q

S/S that indicate alternative diagnosis to Parkinson’s disease (-)

A

□ Onset/course: sudden onset, rapid progression, young onset with strong FHx of other ds
□ Clinical pattern: early and prominent dementia, early frequent falls, early incontinence, no tremor in presence of significant bradykinesia
□ S/S of other causes: pyramidal/cerebellar signs/autonomic dysfx (MSA), gaze palsy (PSP), cortical signs/alien hand syndrome (CBD)
□ Retrospective: poor treatment response to levodopa (PD usually excellent response)

51
Q

Specific imaging for Parkinson’s disease

A

CT/MRI to rule out alternative causes

Dopaminergic SPECT/PET: ↓dopamine activity in basal ganglia: examples:

  • DaT scan (SPECT)
  • 18F-Dopa Scan, 11C- Raclopride PET scan
  • MRI - DTI, DWI, ADC mapping
52
Q

Treatment outline for PD

A

Initial treatment: Levodopa

Adjunctive treatment for dyskinesia or motor fluctuation
Options: dopamine agonist, MAO-B inhibitor, COMT inhibitor

Surgical Tx considered for pharmacologically refractory cases

53
Q

Examples of levodopa-based treatment for PD

A

eg. Sinemet (levodopa + carbidopa), Madopar (levodopa + beserazide)

54
Q

MoA of levodopa + carbidopa/ beserazide (-)

A

MoA:
Levodopa is precursor of dopamine → decarboxylated into dopamine → replenishes inadequate dopamine in striatum

Carbidopa/ Beserazide: Peripheral DOPA decarboxylase inhibitor cannot pass BBB → Decrease peripheral decoration of levodopa → Decrease peripheral side effects, Increase central availability

55
Q

Levodopa S/E

A

→ Nausea, vomiting, orthostatic hypotension

→ Confusion and visual hallucinations

→ Impulse control disorders: eg. compulsive cleaning, gambling, hypersexuality

→ Dopamine dysregulation syndrome/ Addiction: compulsive use of dopaminergic drug (addiction)

56
Q

Outline treatment plan for PD by: (-)

  • Tremor predominant or not
  • Good response to therapy or not
  • Impairment of ADL or not
A
57
Q

Long term Dopamine therapy complications *

A
  1. Loss of efficacy
  2. Motor fluctuations: unpredictable response to levodopa with On and Off episodes
  3. Dyskinesia: Chorea and dystonia in peak-dose or diphasic
  4. Psychiatric complications
58
Q

Adjunct therapy to levodopa for PD

A

Dopamine agonist (DA), eg. rotigotine (skin patch), pramipexole, ropinirole, apomorphine

MAO-B inhibitor (MAOI), eg. selegiline, rasagiline
□ MoA: inhibitor of monoamine oxidase → decrease DA breakdown

Catechol-O-methyltransferase (COMT) inhibitor, eg. entacapone
□ MoA: ↓methylation of dopamine and levodopa → increase duration of action of levodopa

59
Q

Salvage therapy for long-term levodopa use

A

Amantadine:
□ MoA: unknown, likely a/w NMDA receptor blockade
□ Use: treatment of LD-induced dyskinesias

Anticholinergics, eg. orphenidrine, benzhexol (Artane), benztropine
□ MoA: inhibitor muscarinic cholinergic fibres in striatum → ↓inhibition
□ Use: initial therapy in young-onset pt w/ prominent dystonia and tremor

60
Q

2 surgical options for PD

A

Destructive neurosurgery:
→ Thalamotomy for control of medically intractable tremor
→ Pallidotomy for control of LD-induced dyskinesias, rigidity, bradykinesia, tremor

Deep brain stimulation (DBS): medically refractory tremor or motor fluctuation

61
Q

Management options for non-motor symptoms of PD

A

Psychosis: antipsychotics (eg. quetiapine, clozapine, pimavanserin)

PD-Dementia: cholinesterase inhibitor

Depression: desipramine (TCA) and citalopram (Refute most SSRIs)

(SSRIs can interact with MAOI (5HT syndrome) and a/w risk of ↑motor symptoms)

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