Pattern recognition Flashcards

1
Q

What are the features of an upper motor neuron pattern?

A

Increased tone, brisk reflexes, pyramidal/corticospinal pattern of weakness i.e. weak extensors in the arms, weak flexors in the legs

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2
Q

What are the features of a lower motor neuron pattern?

A

Wasting, fasciculation, decreased tone, decreased or absent reflexes, flexor plantars/Babinski sign

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3
Q

What are the features of muscle disease?

A

Wasting (usually proximal), decreased tone, decreased or absent tendon reflexes

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4
Q

What are the features of neuromuscular junction injury?

A
  • Fatiguable weakness, normal or decreased tone, normal tendon reflexes
  • No sensory symptoms
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5
Q

What are the features of functional weakness?

A

No wasting, normal tone, normal reflexes, erratic power, non-anatomical loss

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6
Q

What can cause UMN lesions?

A
  • Acute stroke syndrome, space occupying lesions and spinal cord problems
  • Can usually be determined by body segments involved and accompanying signs e.g, hemispheric - contralateral pyramidal weakness in face, arm and leg
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7
Q

What can cause LMN lesions in the anterior horn cells?

A

Occurs with motor neuron disease, spinal muscular atrophy, lead poisoning, poliomyelitis

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8
Q

What can cause LMN lesions in the peripheral nerves and how does this present?

A
  • Symmetrical polyneuropathy with weakness and sensory symptoms - frequent complication of diabetes. Other causes include alcohol or metabolic insults as well as heritable disorders
  • Mononeuropathy as a result of nerve compression (carpal or tarsal tunnel syndrome, ulnar neuropathy, radial neuropathy) or mononeuritis multiplex which occurs in the context of diabetes or vasculitis
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9
Q

What can cause neuromuscular junction injury and how does it present?

A
  • Presents with purely fatiguable motor symptoms
  • Occurs in acetylcholine receptor antibody mediated myasthenia gravis, inhibition of acetylcholinesterase by organophosphate poisoning, or interference with presynaptic calcium channel function in Lambert-Eaton paraneoplastic syndrome
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10
Q

What can cause muscle disorders and how do they present?

A
  • Often symmetrical, often proximal, very wide differential diagnosis
  • Inflammatory e.g. polymyositis, vasculitis
  • Endocrine e.g. hypothyroidism, Cushing’s
  • Drugs and toxins e.g. alcohol, cocaine, steroids
  • Infections e.g. HIV, pyomyositis, toxoplasmosis
  • Rhabdomyolisis
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11
Q

What nerve and nerve root supplies the deltoid muscle? What movement does the deltoid muscle control?

A

Axillary nerve, C5 nerve root, controls shoulder abduction

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12
Q

What nerve and nerve root supplies the triceps muscle? What movement does the triceps muscle control?

A

Radial nerve, C7, controls elbow extension

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13
Q

What nerve and nerve root supplies the iliopsoas muscle? What movement does the iliopsoas muscle control?

A

Femoral nerve, L1, 2, controls hip flexion

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14
Q

What nerve and nerve root supplies the hamstring muscles? What movement do the hamstring muscles control?

A

Sciatic, S1, controls knee flexion

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15
Q

What nerve and nerve root supplies the peroneal muscles? What movement do the peroneal muscles control?

A

Common peroneal and sciatic, L4, 5, controls ankle dorsiflexion

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16
Q

What nerve and nerve root supplies the extensor hallucis longus muscle? What movement does the extensor hallucis longus muscle control?

A

Common peroneal, L5, controls great toe dorsiflexion

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17
Q

What nerve roots innervate the ankle reflex?

A

S1, 2

18
Q

What nerve roots innervate the knee reflex?

A

L3, 4

19
Q

What nerve roots innervate the biceps reflex?

A

C5, 6

20
Q

What nerve roots innervate the triceps reflex?

A

C7, 8

21
Q

What does a stocking (and later glove) distribution of sensory loss suggest?

A

Length dependent neuropathy

22
Q

What does a sensory level pattern of sensory loss suggest?

A

Spinal cord lesion

23
Q

What does a hemianaesthesia suggest?

A

Contralateral cerebral lesion, or with no other signs a non-organic disorder

24
Q

What does dissociated sensory loss suggest?

A

Loss with lost spinothalamic (pain/temperature) but preserved dorsal column (fine touch, vibration, proprioception) suggests hemicord damage (Brown-Sequard syndrome, syringomyelia, anterior spinal artery syndrome)

25
Q

What are cerebellar signs?

A
  • Cerebellar gait is broad-based and unsteady
  • Intention tremor/ataxia is assessed in the arms by finger-nose test and in the legs by knee-heel testing
  • Dysdiadochokinesis
  • Nystagmus and dysarthria are additional features of cerebellar disorders
  • DANISH - dysdiadochokinesis, ataxia, nystagmus, intention tremor, speech problems, hypotonia
26
Q

What are extrapyramidal symptoms/Parkinsonism?

A
  • Bradykinesia, rigidity, resting tremor, impaired gait and posture
  • Hypomimia
  • Hypophonia
  • Reduced arm swing, stooped posture, small steps, festination, turning en bloc
  • Impaired postural reflexes
  • Asymmetry in PD, symmetry in drug induced or atypical PD
27
Q

What does the frontal lobe control?

A

Generates novel strategies and has executive functions. It enables self-criticism and trying again. The prefrontal cortex connects extensively to other association cortices, basal ganglia, limbic system, thalamus and hippocampus

28
Q

What are some signs associated with frontal lobe dysfunction?

A

Personality dysfunction, paraparesis, paratonia, grasp reflex, seizures, incontinence, visual field defects, expressive dysphasia (Broca’s area), anosmia (olfactory pathway)

29
Q

What are some signs associated with temporal lobe dysfunction?

A

Memory dysfunction, agnosia, receptive dysphasia (Wernicke, dominant hemisphere), visual field defects (superior quadrantopia), auditory dysfunction, limbic dysfunction, temporal lobe epilepsy

30
Q

What are some signs associated with parietal lobe dysfunction?

A

Visual field defect (inferior quadrantopia) sensory dysfunction, Gerstmann’s syndrome (Dysgraphia, left-right disorientation, finger agnosia, acalculia), dyspraxia, inattention, denial

31
Q

What is used to treat Parkinson’s disease?

A

Levodopa - crosses the BBB while dopamine does not, levodopa is then converted into dopamine in the brain

32
Q

What drug is often used concomitantly with levodopa when managing PD?

A

COMT inhibitors - levodopa can be broken down by catechol-O-methyltransferase (COMT) so COMT inhibitors such as entacapone are often used

33
Q

What are the cardinal features of PD?

A
  • Resting tremor, rigidity, bradykinesia and postural instability
  • PD is usually asymmetrical
  • Postural instability leading to falls occurs relatively late in the clinical course of PD
34
Q

What are the cardinal features of multiple sclerosis (MS)?

A
  • Visual compromise, stiffness and weakness
  • MS can have lesions on MRI without clinical compromise directly related to those lesions
  • Oligoclonal bands in the CSF are also found in other conditions
  • The symptoms of MS can worsen with fever
35
Q

Describe the clinical presentation of motor neuron disease

A
  • Progressive muscular atrophy accounts for 10% although most eventually develop UMN signs
  • Primary lateral sclerosis is a pure upper motor syndrome
  • Usually it is a mix of UMN and LMN abnormalities in the absence of sensory disturbances
  • Cognitive impairment may be part of the presentation
  • Ask about cramps, fasciculations, foot drop, family history and behavioural changes
  • Frontotemporal dementia
36
Q

How is imaging used to investigate stroke?

A
  • MRI T1/2 and FLAIR images to identify old lesions and lesions of non-vascular origin
  • Diffusion weighted images to identify new ischaemic lesions
  • T2 to identify bleeds and microbleeds
  • Perfusion weighted images may be useful to identify brain areas at risk of ischaemia
  • CT brain - hyperintensities
37
Q

What are the clinical features of lacunar syndrome?

A
  • No visual field defect, no new higher cortical or brainstem dysfunction
  • Pure motor hemiparesis, or pure sensory deficit of one side of the body, or sensorimotor hemiparesis or ataxic hemiparesis
  • At least 2 of the 3 areas (face, arm, leg) should be involved in its entity
38
Q

What are the clinical features of posterior circulation syndrome?

A

Cranial nerve palsy, unilateral or bilateral motor or sensory deficit, disorder of conjugate eye movements, cerebellar dysfunction, homonymous hemianopia, cortical blindness

39
Q

What are the clinical features of total anterior circulation syndrome?

A

Hemiplegia and homonymous hemianopia contralateral to the lesion and either aphasia or visuospatial disturbances +/- sensory deficit contralateral to the lesion

40
Q

What are the clinical features of partial anterior circulation syndrome?

A
  • One or more of unilateral motor or sensory deficit, aphasia or visuospatial neglect (with or without homonymous hemianopia)
  • Motor or sensory deficit may be less extensive than in lacunar syndrome