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Neurology > Dizziness and Syncope > Flashcards

Dizziness and Syncope Flashcards

1
Q

What is dizziness?

A

transient episode of disturbed consciousness

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2
Q

What is syncope?

A

global reduction in cerebral blood flow causing LOC for short duration (20-30s)

  • Rapid and complete recovery
  • Symptom, not disease
  • Dizziness/faintness is prodromal of syncope
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3
Q

List 5 causes of Cerebellar Syndrome.

A

• Inherited: Friedrich’s Ataxia, Ataxia telangiectasia, MS, Wilson Disease

  • Vascular: Trauma, haemorrhage, oedema, stroke
  • Inflammatory/Idiopathic
  • Toxic: Alcoholism
  • Autoimmune?
  • Metabolic?
  • Infective/Post-infective: Influenza (B), TB,
  • Neoplastic/Paraneoplastic: Haemangioblastomas, medulloblastomas, Gliomas, Cerebellar degeneration

• Endocrine: Thiamine deficiency (Wernicke encephalopathy), Cobalamin deficiency

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4
Q

Outline the pathophysiology of Cerebellar Syndrome.

A

• Causative agent –> lesion/damage in the brain (cerebellum (spinocerebellum pathway)/vestibular apparatus (vestibulocerebellum pathway)/cortex (cerebrocerebellar pathway) –> motor output changed e.g. nystagmus, dysarthria, wide-based gait, dysmetria (finger-nose ataxia), truncal ataxia, dysdiadochokinesia (rapid alternating movement test/rebound phenomenon (Stewart-Holmes Sign), Vertigo

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5
Q

List 5 signs of Cerebellar Syndrome.

A
  • Nystagmus (oculomotor dysfunction)
  • Dysarthria (scanning speech)
  • Cerebellar ataxia: Gait ataxia (wide-based gait)/Truncal ataxia/Limb ataxia
  • Dysmetria: Finger-to-nose test
  • Dysdiadochokinesia (X antagonistic-agonistic motions): Rapid alternating movement test/Stewart-Holmes Sign
  • Pronator drift
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6
Q

What is Idiopathic Parkinson’s Disease?

A

Neurodegenerative disease caused by accumulation of a-synuclein bound to ubiquitin forming cytoplasmic inclusions (Lewy bodies) ≈ depletion of dopamine-secreting cells in substantia nigra. Dopamine-secreting cells in substantia nigra project to striatum thus loss leads to change in activity of neural circuits in basal ganglia regulating movement. Non-striatal pathways affected result in neuropsychiatric pathology associated with PD.

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7
Q

List 3 risk factors of Idiopathic Parkinson’s Disease?

A
  • Genetic: ∆Parkin gene, ∆a-synuclein gene, ∆Ubiquitin carboxyl-terminal hydrolase L1 gene
  • MPTP (Methylphenyltetrahydropyridine): Illegal synthesis of opiates  DIP
  • PMHx Encephalitis lethargica
  • Smoking
  • Heavy metal exposure
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8
Q

Outline the pathophysiology of Idiopathic Parkinson’s Disease.

A

• Misfolded alpha-synuclein in ER –> alpha-synuclein + ubiquitin = Lewy Body –> Lewy Body accumulation in Substantia Nigra ≈

1) Striatal pathway: Depletion of DA neurones of SNc
- -> Reduced activation of D1 neurones to MSN in Striatum which synapse on GABAergic neurones in GPi ≈ reduce direct pathway thus reduced inhibition of GABAergic neurones ≈ reduced motor activity

–> Unopposed cholinergic interneurones ≈ increase indirect pathway via ACh @ D2 MSNs projecting from striatum to GPe then STN ≈ excitatory for inhibitory GABAergic neurones ≈ reduced motor activity

+ Non-striatal pathways…depleted DA neurones ≈ neuropsychiatric pathology associated with PD

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9
Q

Which Dopaminergic neuronal pathway is part of the GPi?

A

Direct

Direct Pathway is D1 receptor MSNs (caudate nucleus and putamen) to GABAergic cells in SNr and GPi –> net excitatory effect

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10
Q

Which Dopaminergic neuronal pathway is part of the GPe?

A
  • Indirect Pathway is D2 receptor MSNs (caudate nucleus and putamen) to GABAergic cells in GPe –> SNr via excitatory STN –> net inhibitory effect
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11
Q

What region of the basal ganglia is primarily affected in Parkinson’s Disease?

A. Caudate

B. Lenticulate

C. Subthalmic

D. Substantia Nigra

A

D. Substantia Nigra

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12
Q

What region of the basal ganglia is primarily affected in Huntington’s Disease?

A. Caudate

B. Lenticulate

C. Subthalmic

D. Substantia Nigra

A

A. Caudate

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13
Q

What region of the basal ganglia is primarily affected in Wilson’s Disease?

A. Caudate

B. Lenticulate

C. Subthalmic

D. Substantia Nigra

A

B. Lenticulate

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14
Q

What region of the basal ganglia is primarily affected in Hemiballismus?

A. Caudate

B. Lenticulate

C. Subthalmic

D. Substantia Nigra

A

C. Subthalmic

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15
Q

What is Juvenile Parkinson’s Disease?

A

• Juvenile Parkinsonism: ≤ 21 years old

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16
Q

What is Young-Onset Parkinsonism?

A

• Young-onset Parkinsonism: 21-40 years old

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17
Q

Give 5 symptoms of Idiopathic Parkinson’s Disease

A
  • Resting tremor: 4-7kHz resting tremor; hands (pill-rolling of thumb and fingers); improved by voluntary movement; worsened by anxiety
  • Rigidity: Increased tone in trunk and limbs; limbs resist passive extension (lead-pipe rigidity or cogwheel if with tremor) cf UMN lesion where resistance falls away with movement (clasp-knife)
  • Akinesia/Bradykinesia: difficult initiation of movement; expressionless face; speech is slow and monotonous; writing is small (micrographia) and tails off at end of line; Slowness of moving; Asymmetry
  • Asymmetry
  • Postural instability: Imbalance; Stooped posture
  • Shuffling gait: Festinant (hurrying) with poor arm swinging ≈ ‘Simian’ due to forward flexion, immobility of arms and lack of facial expression (hypomimia)
  • Hypomimia (lack of facial expression)
  • Micrographia: small hand writing
  • Positive Glabellar Tap: Eyes shut when touching nasal bridge
  • Neuropsychiatric symptoms: Depression/Hallucinations/Dementia/Impulsive disorders
  • Sleep disorders: Insomnia/sleep fragmentation/Vivid dreams
  • Autonomic disorders: Sialorrhea (drooling)/ Diaphoresis/ Dysphagia/Constipation)
  • Anosmia
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18
Q

What investigation is required to diagnose Idiopathic Parkinson’s Disease?

A

• Clinical diagnosis

  • MRI: DaT imaging (radiolabelled ligand binding to dopaminergic terminals –> shows extent of nigrostriatal cell loss)
  • Emission tomography: Dopamine signalling in nigrostriatal pathway
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19
Q

Give the management of Idiopathic Parkinson’s Disease.

A

• Dopamine precursor: Levodopa (taken with Dopa decarboxylase inhibitor)
+
• Dopadecarboxylase inhibitor: Carbidopa

  • Dopamine agonists: Pramipexole/Ropinirol/Rotigotine/Bromocriptine
  • COMT (catechol-O-methyl transferase) inhibitor: Entacapone
  • MAO-B inhibitors: Selegine/Rasagiline
  • Dopamine release enhancer: Amantadine
  • Muscarinic Antagonists: Benzhexol (Trihexyphenidyl hydrochloride)
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20
Q

Which of the following is a Dopadecarboxylase inhibitor?

A. Levodopa

B. Carbidopa

C. Bromocriptine

D. Entacapone

A

B. Carbidopa

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21
Q

Which of the following is a Dopamine precursor?

A. Levodopa

B. Carbidopa

C. Bromocriptine

D. Entacapone

A

A. Levodopa

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22
Q

Which of the following is a Dopamine agonists?

A. Levodopa

B. Carbidopa

C. Bromocriptine

D. Entacapone

A

C. Bromocriptine

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23
Q

Which of the following is a COMT inhibitor?

A. Levodopa

B. Carbidopa

C. Bromocriptine

D. Entacapone

A

D. Entacapone

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24
Q

Which of the following is a MAO-B inhibitor?

A. Levodopa

B. Selegelline

C. Bromocriptine

D. Entacapone

A

B. Selegelline

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25
Q

Which of the following is a Dopamine release enhancer?

A. Levodopa

B. Selegelline

C. Amantadine

D. Entacapone

A

C. Amantadine

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26
Q

Which of the following is a Muscarinic antagonist?

A. Levodopa

B. Selegelline

C. Benzhexol

D. Entacapone

A

C. Benzhexol

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27
Q

What is the precursor for Dopamine production?

A

Tyrosine

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28
Q

What is the MOA of Levodopa?

A

Dopamine precursor when combined with Carbidopa (Dopacarboxylase inhibitor)
• Improve rigidity
• Improve hypokinesia
• Little evidence for slowing or accelerating neurodegeneration

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29
Q

List 3 side effects of Levodopa

A
  • Dyskinesia: Involuntary writhing movements (2 years after); affect face and limbs mainly; occurs at peak therapeutic effect
  • Fluctuations in clinical state
  • Hypokinesia and rigidity may suddenly worsen then improve ≈ receptor dynamics
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30
Q

Give the MOA of Bromocriptine and Cabergoline

A

orally active; work on D1 and D2 receptors

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31
Q

Give the MOA of Pramipexole or Roprinole?

A

orally active D2/D3 receptor agonists; short half life

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32
Q

What Dopamine agonist can be administered as a transdermal patch?

A. Bromocriptine

B. Apomorphine

C. Cabergoline

D. Rotigotine

A

D. Rotigotine

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33
Q

List 3 side effects of Dopamine agonists such as Bromocriptine, Cabergoline, Pramipexole and Rotigotine.

A
  • Sudden onset sleep
  • Impulse control disorders: Gambling, Binge Eating, Hypersexuality
  • Hypotension
  • Neuroleptic malignant syndrome if abrupt ending
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34
Q

What drug can be administered as an injection to control the off-effects of Levodopa?

A

Apomorphine

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35
Q

Give an example of a MAO-inhibitor used to treat Parkinson’s disease.

A
  • Selegiline: selective MAO-B inhibitor = no SEs; increase dopamine levels
  • Rasagiline: Alternative MAO-B inhibitor; may retard disease progression
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36
Q

Which antiviral drug can be beneficial in PD as a levodopa release enhancer?

A

Amantidine

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37
Q

Give an example of a Acetylcholine antagonist.

Give the side effects of this drug.

A

• Benzhexol/Orphenadrine/Procyclidine

SEs: Anti-cholinergic side effects
•	Altered level of consciousness: hallucination/word salad/delirium/coma 
•	Seizures 
•	Sinus tachycardia 
•	Hypertension
•	Hyperthermia (low-grade fever)
•	Dry skin (anhydrosis) 
•	Mydriasis 
•	Dry mouth
•	Decreased bowel sounds/peristalsis
•	Constipation
•	Urinary retention
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38
Q

What is Drug-Induced Parkinsonism?

A

Parkinsonian syndrome induced by drugs

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39
Q

Outline the pathophysiology of Drug-Induced Parkinson’s Disease.

A

• MPTP, Reserpine, Phenothiazines, Butyrophenones block Dopamine receptors –> Parkinsonian Syndrome = bradykinesia/akinesia; little resting tremor

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40
Q

Give the investigations you may order to aid your differential of Drug-Induced Parkinson’s Disease.

A
  • Clinical diagnosis

* MRI: DaT imaging (radiolabelled ligand binding to dopaminergic terminals  shows extent of nigrostriatal cell loss)

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41
Q

Give the management of Drug-Induced Parkinson’s Disease.

A

• Remove offending drugs (MPTP/Reserpine/Phenothiazine/Butyrophenone)

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42
Q

What is Benign Essential Tremor?

A

Familial (autosomal dominant) tremor of arms and head (titubation) occurring most frequently in elderly people

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43
Q

Give the main feature of Benign Essential Tremor?

A

Tremor: Exaggerated on activity; Worsened by anxiety; Improved by alcohol, propranolol, primidone (anticonvulsant) and mirtazapine (antidepressant)

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44
Q

Outline the management of Benign Essential Tremor?

A
  • Observation: Mild cases not causing dysfunction or embarrassment
  • Propanalol/Primidone
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45
Q

What is a Chorea?

A

continuous flow of jerky, quasi-purposive movements fitting from one part of the body to another caused by numerous diseases

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46
Q

What is Huntington’s Disease?

A

Rare autosomal dominant condition involving CAG triplet repeat disease (> 40 repeats) with full penetrance causing accumulation of huntingtin primarily in the striatum which is neurotoxic causing neurodegeneration.

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47
Q

Outline the pathophysiology of Huntington’s Disease.

A

• Expanded CAG repeats (>40) –> mutant huntingtin protein ≈ toxic –> cross-linked huntingtin aggregates interfere with mitochondrial energy metabolism + cellular function –> primarily affects striatum ≈ depletion of GABA and ACh but spares dopamine

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48
Q

Give a risk factor of Huntington’s Disease.

A
  • Expansion of CAG repeat length at N-terminal of huntingtin gene
  • FHx
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49
Q

Give 5 symptoms of Huntington’s Disease.

A
  • Impaired work or school performance
  • Personality change
  • Chorea
  • Twitching or restlessness
  • Loss of coordination
  • Deficit in fine motor coordination
  • Slowed rapid (saccadic) eye movements
  • Impaired tandem walking
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50
Q

What investigations might you order to confirm your differential diagnosis of Huntington’s Disease?

A
  • Clinical diagnosis
  • CAG repeat testing: X > 40 CAG repeats
  • MRI/CT Scan: Caudate or striatal atrophy apparent
51
Q

Outline the management of Huntington’s Disease.

A
  • Counselling for family and patient
  • Tetrabenazine (Chorea)
  • Citalopram: 20mg PO OD for 2 weeks then 40mg OD (low mood)
52
Q

What is hemiballismus?

A

Violent swinging movements of one side of body due to damage of contralateral subthalamic nucleus (STN), reducing activity of subthalamic nucleus of basal ganglia –> flailing, ballistic, undesired movements of the limbs

53
Q

Give two causes of Hemiballismus.

A
  • Infarction

* Haemorrhage

54
Q

What is myoclonus?

A

sudden, involuntary jerking of single muscle group/group of muscles

55
Q

What are tics?

A

brief, repeated stereotypical movements, usually involving face and shoulders.

56
Q

What is a dystonia?

A

Prolonged spasms of muscle contraction

57
Q

What is a spasm of forced blinking?

A

• Blepharospasm

58
Q

What is a spasm of head turning?

A

• Spasmodic torticollis

59
Q

What is a spasm of sustained upward gaze?

A

• Oculogyric crises

60
Q

What is an oculogyric crisis?

A

episodes of sustained upward gaze

61
Q

What is a spasmodic torticollis?

A

head turned and held to one side or drawn backwards/forwards

62
Q

What is a blepharospasm?

A

spasms of forced blinking

63
Q

What is the management of Dystonia?

A

Anticholinergic

  • Benztropine: 1-2mg IM or IV
  • Procyclidine: 5mg IM or IV
64
Q

What is Multiple Sclerosis?

A

chronic debilitating autoimmune disorder of CNS with multiple plaques of demyelination within brain and spinal cord. Plaques are disseminated both in time and place.

65
Q

Give 2 classifications of Multiple Sclerosis.

A
  • Relapsing-remitting MS (RMMS) (85-90%): symptoms occur in attacks (relapses) over day and recover over weeks. May accumulate over time –> disability
  • Secondary progressive MS: gradual worsening slowly over years from RRMS
  • Primary progressive MS (PPMS) (10-15%): gradually worsening disability without relapses or remissions, presenting later and associated with fewer inflammatory changes
  • Relapsing-Progressive MS (< 5%): Similar to PPMS but occasional relapses on background of progressive disability from outset
66
Q

Give 2 risk factors for Multiple Sclerosis.

A
  • Female
  • 20-40 years
  • Northern hemisphere
  • Hypocalcemia
67
Q

Give 3 aetiological factors of Multiple Sclerosis.

A
  • FHx MS: HLA and IL (?)
  • Toxins
  • Viral exposure: EBV infection
  • Sunlight exposure (and effect on vitamin D metabolism): strong correlation
68
Q

What viral pathogen is putatively linked as an aetiological cause of Multiple Sclerosis.

A

Epstein-Barr Virus

69
Q

Outline the pathophysiology of Multiple Sclerosis.

A

• Trigger –> Lymphocytes with encephalitogenic potential activated –> attachment to endothelial cells @ VCAM ≈ MMPs and cytokine activation –> breach in BBB –> inflammatory infiltration ≈ T-cells produce inflammatory cytokines causing toxicity and attracting macrophages –> damage ≈ sclerosis with recovery process: shadow plaques (myelin re-deposition) –> further damage…demyelination ≈ multifocal areas of demyelination, loss of oligodendrocytes, astrogliosis with loss of axons in white matter of CNS

70
Q

State the main pathological consequences of MS plaques

A 
Pathology: MS Plaques
•	Inflammation
•	Demyelination
•	Axonal loss 
•	Sites (CNS): Optic nerves, Periventricular white matter, brainstem, cerebellar connections and cervical spinal cord 
--> Peripheral nerves X affected
71
Q

Give 5 clinical features of Multiple Sclerosis.

A

• Visual disturbance (unilateral): Blurring, pain on moving eye  Optic neuropathy (optic neuritis/optic atrophy/ retrobulbar neuritis)
• Peculiar sensory phenomena: Patch wetness/burning/paraesthesia/tingling
- Lhermitte’s Sign (electric shock-like extending down cervical spine  limbs)
- Trigeminal neuropathy/neuralgia possible
• Foot dragging: Gradual onset of weakness
• Leg cramping: Involuntary movement with cramping in calves, worsens at night or activity
• Fatigue
• Vertigo
• Dysphagia
• Dysarthria
• Pins and needles
• Spastic paraparesis

  • Spasticity/increased tone (UMN)
  • Hyperreflexia (UMN)
  • Gait ataxia (wide-based gait)/Limb ataxia
  • Facial weakness
  • Bilateral internuclear ophthalmoplegia
72
Q

What is the eponymous clinical feature of Multiple Sclerosis which involves electric shocks down the cervical spine to the limbs?

A

Lhermitte’s Sign

73
Q

What is the acute management of Multiple Sclerosis?

A

• Steroids (short-course): Methylprednisolone 1000mg/day for 3 days

74
Q

What is the first line treatment for Multiple Sclerosis?

A. Methylprednisolone

B. Dimethyl fumarate

C. G;atiramer acetate

D. Natalizumab

A

B. Dimethyl fumarate

75
Q

What are the side effects of Dimethyl Fumarate?

A

LFT derangement

Nausea

Alopecia

76
Q

What is the MOA of Glatiramer acetate?

A

Compete with myelin antigens for presentation to T cells

77
Q

What is the MOA of Natalizumab?

A

Reduce VCAM adhesion and inflammatory infiltrate IV mont

78
Q

State the risk factors of Natalizumab.

A
  • PML risk

- Increased PML risk if JC +ve or previous immunotherapy

79
Q

What is the MOA of Alemtuzumab?

A

Target T and B cells reducing myelin infiltration

80
Q

State the main side effect of Alemtuzumab.

A

Autoimmune

Thyroid function derangement

Idiopathic Thrombocytopenia

Autoimmune kidney disease

Infection

81
Q

What are the main types of ‘dizziness’?

A
  1. Vertigo
  2. Disequilibrium
  3. Presyncope
  4. Postural symptoms
82
Q

Give the two types of vertigo.

A

i) Peripheral (Vestibular)
• Hearing loss and tinnitus
• Sudden onset
• Associated with rotary illusions (nausea + vomiting)
• Nystagmus combined horizontal and rotational; lessens when gaze is focused
• Mild to moderate imbalance

ii) Central
• Vertigo develops gradually
–> Exception: Acute cerebrovascular events (an acute central vertigo)
• Central lesions  neurological Sx and signs
• Auditory features uncommon

83
Q

Give 3 common causes of Vertigo.

A
  • BPPV: Loose otoconia particles in semi-circular canals – usually posterior semi-circular canals
  • Meniere’s disease: Idiopathic; associated with endolymphatic hydrops  tinnitus + hearing loss + vertigo
  • Labyrinthitis: acute infection of vestibular organs
  • Vestibular neuritis: acute peripheral vestibulopathy due to reactivation of viral infection (HZV) affecting vestibular ganglion, vestibular nerve, labyrinth or combination
84
Q

Give 3 common causes of Disequilibrium.

A
  • Peripheral neuropathy
  • Eye Disease
  • Peripheral vestibular disorders
85
Q

What is presyncope?

A

Lightheadedness without sensation of movement as a prodrome of syncope (fainting) due to conditions reducing cerebral blood flow

86
Q

What is disequilibrium?

A

feeling of unsteadiness or instability/off balance

87
Q

What is lightheadedness? What clinical test can you use to differentiate if the lightheadedness has a distinct, clinical cause?

A

Psychophysiological or psychogenic dizziness occurs spontaneously
–> Romberg test (clinical balance test): Normal but then walking across the room they are dizzy

88
Q

Give two examples of types of lightheadedness.

A
  • Psychogenic dizziness: Panic disorder with agoraphobia, personality disorders and generalized anxiety
  • Phobic postural vertigo: Dizziness in standing and walking despite normal clinical balance test + anxiety/avoiding behavior
89
Q

What is BPPV?

A

common cause of vertigo involving loose otoconia particles in the semi-circular canals (commonly posterior or lateral semi-circular canals) which results in peripheral vertigo.

90
Q

Give 3 clinical features of BPPV

A
  • Episodic vertigo
  • Triggers/Onset: Rolling in bed/looking up
  • Duration: Seconds
91
Q

Give the main investigation find in BPPV.

A
  • Dix-Hallpike: Positive if nystagmus

* Pure tone audiogram: Normal (investigation of exclusion)

92
Q

Outline the management for BPPV.

A

• Epley Maneuver

93
Q

What is Meniere’s Disease?

A

Auditory disease characterized by episodic onset of symptomatic triad: Vertigo, hearing loss and roaring tinnitus with a sensation of pressure/discomfort in the affected ear

94
Q

Give a risk factor for Meniere’s Disease.

A
  • Increased age > 40 years
  • FHx
  • Recent viral illness
  • Autoimmune disorders
95
Q

Give the main clinical features of Meniere’s Disease.

A
  • Nausea + Vomiting
  • Roaring tinnitus
  • Vertigo (peripheral): 20 minutes to 12 hours
  • Hearing loss
  • Fullness in affected ear: Pressure/discomfort in the affected ear
96
Q

Outline the investigations you may wish to conduct to support a differential of Meniere’s disease?

What might you want to rule out?

A
  • Clinical diagnosis
  • Pure tone audiogram: Sensorineural hearing loss (low frequencies)
  • MRI: Normal – exclude acoustic neuroma
97
Q

Outline the management of Meniere’s Disease.

A

• Low salt diet: < 6g per day
–> Reduce endolymph
• Thiazide Diuretics: Acetazolamide/Hydrochlorothiazide
–> Reduce endolymph
• Physiotherapy: Vestibular and balance rehabilitation therapy
• Meniett device: TDS –> intermittent pressure pulses through ear canal ≈ reduce vertigo

98
Q

What is Vestibular neuritis?

A

acute peripheral vestibulopathy due to reactivation of viral infection (commonly HSV) affecting vestibular ganglion, vestibular nerve, labyrinth or combination

99
Q

What viral pathogen can be a cause of Vestibular Neuritis?

A

HSV

100
Q

What are the clinical features of Vestibular Neuritis?

A
  • Nausea + Vomiting
  • Vertigo: Acute onset lasting for days
  • Nystagmus
  • Abnormal head impulse test: Loss of vestibulo-ocular reflex
101
Q

How is the diagnosis of vestibular neuritis made?

A

• Clinical diagnosis

102
Q

What is used to manage vestibular neuritis?

A

• Corticosteroids

103
Q

What is labyrinthitis?

A

inflammatory condition affecting the labyrinth in the cochlear and vestibular system of the inner ear. Viral labyrinthitis typically precedes an URTI caused by numerous pathogens: HZV/CMV/Mumps/Measles/Rubella/ HIV. Bacterial labyrinthitis associated with: acute/chronic otitis media/meningitis/cholesteatoma. Labyrinthitis may be a feature of autoimmune diseases.

104
Q

Give 3 potential pathogens which may cause labyrinthitis.

A

HZV

CMV

Mumps

Measles

Rubella

HIV

Meningitis (Neisseria meningitidis)

105
Q

Give 3 features of Labyrinthitis.

A
  • Vertigo: Acute onset
  • Recent infection: preceding acute otitis media
  • Nausea + Vomiting
  • Hearing loss
  • Tinnitus
  • Horizontal nystagmus
  • Otitis media signs
106
Q

What is the management of Labyrinthitis.

A
  • Anti-emetics: Metoclopramide

* Vestibular suppressants: Anticholinergics/Anti-histamines/Benzodiazepines

107
Q

What is an Acoustic Neuroma?

A

Benign, slow growing neoplasm of Schwann cells of CN 8 (Vestibulocochlear nerve). Lesions usually located in internal auditory canal or cerebellopontine angle causing compression of vestibular nerve –> deafness.

108
Q

An acoustic neuroma affects which cranial nerve primarily?

A

CN VIII

Vestibulocochlear Nerve

109
Q

Give 3 clinical features of an Acoustic Neuroma.

A
  • Unilateral sensorineural deafness: Slow onset – months to years
  • Sudden hearing loss
  • Vertigo: Mild
  • Tinnitus
  • Occipital pain on side of the tumour
  • Depression of corneal reflex (CN V damage)
  • Facial pain, paraesthesia and numbness (CN V damage)
  • Dysphagia (CN IX/X/XI damage)
  • Dysphonia/Voice change (CN IX/X/XI damage)
  • Palatal weakness (CN IX/X/XI damage)
110
Q

Outline the management of an Acoustic Neuroma.

A

• Referral to ENT/Oncology

111
Q

A 57 year old man presents with unilateral deafness, sudden hearing loss and mild dizziness which is determined to be a peripheral vertigo. He describes ringing in his ear and occipital pain on the same side as the deafness.

O/E there is facial paraesthesia, occipital pain on the side of deafness and palatal weakness.

His blood tests are unremarkable but the MRI shows a lesion appearing to be in the internal auditory canal.

What is your differential?

What is your management?

A

Acoustic Neuroma

• Referral to ENT/Oncology

112
Q

A 28 year old presents with acute dizziness which is determined to be vertigo. He has recently had an infection as well as experiencing nausea and vomiting. He describes extreme dizziness which is impeding ADL.

O/E you identify hearing loss and tinnitus in the right ear as well as horizontal nystagmus.

What is your differential?

Outline your management plan.

A

Labyrinthitis

  • Anti-emetics: Metoclopramide
  • Vestibular suppressants: Anticholinergics/Anti-histamines/Benzodiazepines
113
Q

A 24 year old male presents with nausea and vomiting in the wake of recent vertigo which began acutely and has lasted for several days.

O/E you identify nystagmus and an abnormal head impulse test.

What is your differential?

Outline your management.

A

Vestibular Neuritis

Corticosteroids

114
Q

A 54 year old gentleman presents with nausea and vomiting. Recently he has had a roaring, ringing sound in his ears experienced dizziness which has lasted for several hours. Additionally, he has been told by his wife that his hearing has diminished. Finally, he feels a pressure/discomfort in his affected ear.

What is your differential?

Outline your management plan for this patient.

A

Meniere’s Disease

• Low salt diet: < 6g per day
-> Reduce endolymph
• Thiazide Diuretics: Acetazolamide/Hydrochlorothiazide
-> Reduce endolymph
• Physiotherapy: Vestibular and balance rehabilitation therapy
• Meniett device: TDS  intermittent pressure pulses through ear canal ≈ reduce vertigo

115
Q

A 62 year old man presents with episodic vertigo which lasts several seconds. He says it mainly occurs when he gets up or moves too fast.

O/E you identify eye movements when conducing a Dix-Hallpike manoeuvre.

What is your differential?

Outline your management for this patient.

A

Benign Paroxysmal Positional Vertigo

• Epley Maneuver

116
Q

A 48 year old lady presents with blurring of her vision and sense of tingling. She says recently she has struggled to walk and noticed her foot was heavier, as if it was dragging. Additionally she described feelings of dizziness which lasts for several minutes then disappear. She also describes feelings of electric shock-like extending down the cervical spine and to the limbs.

She has previous exposure to unknown toxins due to living near an industrial chemical site as well as living most of her life in North Scotland. She says heart conditions run in her father’s side but this rare nerve/movement disease runs in her mother’s side, she cannot remember what it is called.

O/E you notice spasticity in her muscle, hyperreflexia, gait ataxia and bilateral internuclear ophthalmoplegia (impaired abduction).

Investigation show low calcium normal TSH, normal FBC and MRI-brain shows hyper intensities in the periventricular white matter.

What is your differential?

Outline the management for this patient.

A

Multiple Sclerosis

Acute: Methylprednisolone

Ongoing

1st

  • Dimethyl fumarate
  • Beta-interferon
  • Glatrimer Acetate

2nd

  • Natalizumab
  • Ritixumab/Ocrelizumab

3rd

  • Natalizumab
  • Alemtuzumab
  • Mitoxantrone
  • Autologous Stem Cell Transplantation
117
Q

A 32 year old male presents with violent swinging movements unilaterally. He recently had a stroke.

What is your differential for this sign?

A

Hemiballismus

118
Q

A patient presents with sudden, involuntary jerking of muscles in his arm.

What is this symptom known as?

A

Myoclonus

119
Q

A patient presents with brief, repeated movements usually in his face and shoulders.

What is this symptom known as?

A

Tics

120
Q

A 45 year old woman presents with a continuous flow of jerky movements from her arms to her legs and twitching. She describes a recent loss of coordination (dyspraxia) and a deficit in her fine motor coordination.

She is healthy otherwise with no remarkable PMHx. She has worked as a Teacher for 20 years and does not smoke or drink alcohol. She says her estranged mother passed away from a nervous condition but she cannot remember what from.

O/E you notice saccadic eye movements, a twitching and a chorea.

Her investigation comes back showing numerous repeats trinucleotides in a specific region of her genome.

What is your differential?

Outline the management plan.

A

Huntington’s Disease

  • Citalopram/Escitalopram/Fluoxetine
  • Tetrabenzine (VMAT-2 inhibitor)
121
Q

A 55 year old man presents with a tremor of the arms. He says the tremor has begun to worsen but is exaggerated on activity, worsened by anxiety and worsened by stress. He does not smoke, drinks 10 units of alcohol per week but says the alcohol seems to help his tremor.

O/E you notice the tremor. However, there is no cog-wheeling of the elbow, no rigidity, no postural instability or akinesia.

What is your differential?

Outline your management plan for this patient.

A

Benign Essential Tremor

  • Supportive: CBT/Mindfullness
  • Propanolol
122
Q

A 64 year old ex-construction worker presents with a resting tremor which has gotten worse in the last 3/12. He also describes slower movement of late as well as more stiff-feeling muscles. Finally, he is concerned that he will have a fall and feels a bit off-balance regularly which concerns him. He also says he has had difficulty sleeping recently due to sleep fragmentation nd insomnia.

He is retired now, currently smokes with 50 pack years and has had experience to heavy metals in his profession.

O/E you notice hypomimia and his shuffling gait when he enters the examination room. You observe a resting tremor with pill-rolling of hands and fingers. You identify cog-wheeling in the elbow and observe a bradykinesia.

His bloods are unremarkable but an MRI-Head using DaT technology shows radiolabelled ligand binding to dopaminergic terminals.

What is your differential?

Outline the management options

A

Idiopathic Parkinson’s Disease

Levodopa

Carbidopa

Pramipexole/Bromocriptine

Entacapone

Selegilline/Rasagilline

Amantadine

Benzhexol

123
Q

A 37 year old homeless man presents with a resting tremor which gets better when performing a task. He describes loss of balance, slowness of movement and muscle rigidity.

He has had no exposure to toxic metals but is a regular smoker which is usually street drugs such as Heroine, Crack Cocaine or Cannabis. He says he recently tried a new street drug called MP-TeaPee which is modelled of a Native American bush plant. He says several of his friends have experienced similar symptoms.

What is your differential diagnosis?

Outline your management

A

Drug-Induced Parkinson’s Disease

Remove the offending drug
± Parkinson’s Treatment

  • Levodopa
  • Carbidopa
  • Pramipexole/Bromocriptine
  • Entacapone
  • Selegilline/Rasagilline
  • Amantadine
  • Benzhexol

Neurology (8 decks)

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