Differential diagnosis Flashcards

clinical imaging

1
Q

What is PD

A
  • Motor (Cardinal Sx)- Bradykinesia, rigidity, tremor, postural instability
  • Neuropsychiatric: Dementia, depression, anxiety, delusion, hallucination, psychosis
  • Sleep disturbances: RLS, EDS
  • Sensory: Pain, hyosmia, visual Sx
  • Autonomic: Urinary frequency/urgency, Nocturia, sweating, Orthostatic hypotension, ED
  • GI: Sialorrhoea, Dysphagia, gastroparesis, constipation
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2
Q

Degenerative causes of parkinsonism

A
  • Synucleinopathies: PD, MSA (multisystem atrophy), DLB (Dementia with lewy bodies)
  • Tauopathies: PSP, CBD
  • Vascular

Synuclein and Tau are proteins they build and cause the various diseases

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3
Q

Non-degenerative causes

A
  • Drug induced
  • Metabolic
  • Infective
  • Structural
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4
Q

Causes of tremor

A
  • Essential tremor (most common)
  • Thyrotoxicosis
  • Neuropathic
  • Drug induced
  • Task specific
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5
Q

UK Brain bank criteria

A

1) Diagnosis a parkinsonian syndrome: Must have bradykinesia plus at least 1 of the 3 other cardinal Sx (Rigidity, rest tremor, postural instability)
2) Exclusion Criteria
3) Supportive prospective positive criteria: Must have 3 or more for definitive diagnosis

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6
Q

2) Exclusion criteria

A
  • repeated strokes with stepwise progression- think vascular parkinsons
  • repeated head injury
  • antipsychotic or dopamine-depleting drugs
  • definite encephalitis and/or oculogyric crises on no drug treatment
  • more than one affected relative
  • sustained remission
  • negative response to large doses of levodopa (if malabsorption excluded)
  • strictly unilateral features after 3 years
  • other neurological features: supranuclear gaze palsy, cerebellar signs, early severe autonomic involvement, Babinski sign, early severe dementia (DLB) with disturbances of language, memory or praxis
  • exposure to known neurotoxin
  • presence of cerebral tumour or communicating hydrocephalus on neuroimaging
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7
Q

3) Supportive prospective positive criteria

A
  • unilateral onset
  • excellent response to levodopa
  • rest tremor present
  • severe levodopa-induced chorea
  • progressive disorder
  • levodopa response for over 5 years
  • persistent asymmetry affecting the side of onset most
  • clinical course of over 10 years
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8
Q

A good approach

A
  1. History + Exam
  2. Identify PD- Bradkinesia +
  3. Exclude red flags
  4. Supportive non-motor features
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9
Q

Red flags

A
  • Traumatic head injury
  • Repeated Strokes
  • Culprit medications
  • Symmetrical onset
  • Early falls
  • Early dementia
  • Early autonomic dysfunction
  • Rapid progression
  • Poor Tx response
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10
Q

Supportive non-motor Sx

A
  • Hyposmia
  • Constipation
  • Anxiety
  • Depression
  • Apathy
  • Sleep disturbances
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11
Q

Essential tremor

A
  • Action tremor
  • Postural tremor
  • Head tremor
  • Vocal tremor
  • Often bilateral (PD usually starts unilaterally and develops bilaterally over many years)
  • Improved by alcohol (not always)
  • Treatment: Beta-blockers, anti-epileptics, rarely surgery
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12
Q

Atypical Parkinsonian Syndromes

A
  • Progressive supranuclear palsy (PSP)
  • Multi System Atrophy (MSA)
  • Cortico-basal degeneration (CBD)
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13
Q

PSP Sx

A
  • Predominately symmetrical
  • Early postural instability and falls (backwards)
  • Retrocollis (Neck extensions)
  • Frontalis Overactivity (startled expression)
  • Bradyphrenia (delayed thoughts then delayed speech)
  • Dementia
  • Frontal dysfunction- verbal fluency, luria test, applause sign
  • Axial rigidity- rigidity in the torso
  • Growling dysarthia & Dysphagia- husky voice
  • Poor L-dopa response (normally 600mg of L-dopa before saying non-responsive)
  • Eye signs
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14
Q

Eye signs in PSP

A
  • Supranuclear gaze palsy- Struggle looking veritcally, dolls eye manoeuvre
  • Reduced blink frequency
  • Blepharospasm
  • Square wave jerks
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15
Q

MSA Sx

A
  • Early autonimic features: Orthostatic hypotension (Large drops), urinary rentention, erectile dysfunction
  • Laryngeal dystonia, stridor and sleep apnoea
  • High pitched voices
  • Antecollis (Neck flexion)
  • Stimulus sensitive myoclonus (stretch arms out, flick their outstretch finger you will see lots of myoclonic fasiculations
  • Cognitively intact
  • Poor L-dopa response
  • Several Phenotypes: MSA-P (Parkinsons), MSA- C (Cerebellar)
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16
Q

CBD Sx

A
  • Asymmetrical rigidity and bradykinesia
  • Usually affects 1 limb
  • Apraxia
  • Progressive dystonia, abnormal posturing (limbs in weird positions often their hands)
  • Alien limb (their limb doesn’t feel like their own), inter-manual conflict (their other limbs will try and pull the abnormal posturing back into position)
  • Myoclonus
  • Difficulty in initiating horizontal eye movements
  • Dementia
17
Q

Atypical parkinsonian syndrome key hooks

A
  • PSP: eye signs, falls backwards
  • MSA: Autonomic failure
  • CBD: Apraxia (difficulty performing tasks), dystonia (unintentional sustained muscle contraction resulting in abdnormal posture), alien limb
18
Q

Dementia with lewy bodies

A
  • 80% of people with PD will ultimately develop cognitive impairment many will turn into a dementia
  • If someone has PD for many years then develops dementia that is called ‘Parkinsons disease dementia’
  • If someone develop PD motor symptoms and dementia within a year of eachother that is dementia with lewy bodies
  • Both has visual hallucinations, cognitive fluctuations and daytime somnolence
    *
19
Q

Vascular Parkinsonism

A
  • Multiple cerebral infarct state
  • Small stepping/shuffling gait
  • Few upper limbs signs
  • Poor L-dopa response
  • Stepwise decline
  • Other features of multi-infarct state: Cognitive impairment, incontience, stroke
  • Basal ganglia on CT/MRI is NOT diagnostic- common in older adults
20
Q

Imaging in suspected PD

A
  • Supportive as opposed to diagnostic
  • May not always be necessary
  • Needs to be interpreted alongside the clinical evaluation
  • The indication for the test must be clear
21
Q

Imaging functional vs structure

A
  • Structural= CT + MRI
  • Functional= DAT + PET
22
Q

Structural imaging in PD

A
  1. CT is primarily used to exclude other pathology
    * Multiple infarct state
    * Normal pressure hydrocephalus
    * Space occupying lesion
  2. MRI better for looking at brainstem and cerebellar atrophy.
    - DWI may be helpful
    - May help differentiate PSP & MSA from PD
    - MSA you can see ‘Hot Cross Bun’ sign due to pontine atrophy
    - PSP you can see ‘Hummingbird’ sign (sagital plan) and ‘Mickey Mouse’ sign (transverse plain)- both signs of midbrain atrophy
23
Q

Functional Imaging

A
  1. DAT scan- usually clinical
    * Tracers bind to the dopamine transporter proteins (DAT) in the nigrostriatal nerve endings
    * Uptake is reduced in degenerative PD
    * Can be considered when essential tremor can not distinguished from PD
    * Normal in essential tremor + Drug induced. Abnormal in PD, PSP, DLB, CBD, MSA but will not distinguish between these
  2. PET- usually research
    - Isotopes are made immediately before use 18F-dopa
24
Q

When to use DAT

A
  • If an essential tremor has been stable for years but has changed
  • If someone is on long-standing neuroleptic drugs: can have drug unmasked PD where you need to distinguish between EPSE and somone on for example antipsychotics but is developing underlying PD
  • Someone with sutble signs: slightly bradykinesia +/- other Sx.
  • When questioning atypical
25
Q

Is DAT a good test

A
  • Sensitivity: how good is it at picking up people with the disease (High avoids false negatives e.g. missed cases)
  • Specificity: how good is it at correctly identifying those without the disease (high avoids false positives)
  • PD vs ET= specific and sensitive
  • PD vs APS= low specificity and high sensitivity