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Neurology > Clinical Signs > Flashcards

Clinical Signs Flashcards

1
Q

How does cavernous sinus syndrome cause abducens nerve palsy?

A

Cavernous segment of the abducens nerve is located adjacent to the cavernous carotid artery, and is prone to compression by aneurysmal dilation of the vessel.

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2
Q

What is anosmia?

A

Anosmia is absence of the sense of smell.

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3
Q

What is hyposmia?

A

Decreased ability to recognise smells

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4
Q

What are main causes of anosmia?

A
  • Upper respiratory tract infection (URTI)
  • Chronic allergic or vasomotor rhinitis
  • Trauma
  • Cigarette smoking
  • Normal ageing
  • Alzheimer’s disease
  • Meningioma
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5
Q

What are causes of an ataxic gait?

A
  • Intoxication – alcohol
  • Drug toxicity – lithium, phenytoin, benzodiazepine
  • Cerebellar infarction
  • Vertebral artery dissection
  • Cerebellar mass lesion – tumour, abscess, AVM
  • Multiple sclerosis
  • HSV cerebellitis
  • Hereditary cerebellar degeneration (Freidreich’s ataxia)
  • Paraneoplastic cerebellar degeneration
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6
Q

What cerebellar structures are involved in someone who has truncal ataxia, diequilibrium and body sway?

A

Midline cerebellar structures

  • Vermis
  • Flocculonodular lobes
  • Intermediate lobe
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7
Q

What might a lesion in the flocconodular lobe cause in terms of clinical signs?

A
  • Multidirectional truncal instability
  • Disequilibrium
  • Severe impairment of trunk coordination
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8
Q

What are features of lateral cerebellar hemisphere dysfunction?

A

Ipsilateral abnormalities in:

  • Coordinated leg movements
  • Step timing, length and direction - typically slow and careful, and instability is accentuated during heel-to-toe walking.

Associated features

  • Dysmetria
  • Dysdiadochokinesis
  • Intention tremor
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9
Q

What is dysmetria?

A

Dysmetria is a disturbance of the rate, range and force of movement of the extended limb as it approaches a target. Dysmetria is elicited during the finger-to-nose and heel-to-shin tests

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10
Q

What is dysmetria a sign of?

A

Dysmetria is a cerebellar sign

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11
Q

What causes dysmetria?

A

Lesions of the intermediate and lateral cerebellar hemispheres may cause slow, uncoordinated and clumsy movements of the ipsilateral distal extremity during attempted target localisation tasks. Delays in motor initiation and movement termination, and abnormalities of movement force and acceleration, contribute to dysmetria

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12
Q

What are causes of muscle atrophy?

A
  • Muscle disuse – fracture, arthritis, prolonged immobility
  • Lower motor neuron (LMN) disorders - Peripheral neuropathy, Radiculopathy, Motor neuron disease
  • Peripheral vascular disease
  • Poliomyelitis
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13
Q

How do lower motor neuron lesions cause muscle atrophy?

A

Loss of lower motor neuron input at the neuromuscular junction causes breakdown of actin and myosin, resulting in a decrease in cell size and involution of myofibrils

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14
Q

What is a positive babinski’s response?

A

The Babinski response, or upgoing plantar response, is an abnormal cutaneous reflex of the foot associated with upper motor neuron dysfunction. In a positive Babinski response, scratching the lateral plantar surface of the foot causes contraction of the extensor hallucis longus muscle and extension of the great toe.

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15
Q

What are causes of a positive babinski’s response?

A

Upper motor neuron lesions

  • Cerebral infarction
  • Cerebral haemorrhage
  • Spinal cord injury
  • Lacunar infarction, posterior limb internal capsule
  • Multiple sclerosis
  • SOL
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16
Q

What is thought to be the mechanism behind the development of the babinski response?

A

Before 1 or 2 years of age, a stimulus applied to the lower extremities, such as pressure or stroking of the plantar aspect of the foot, causes involuntary ankle dorsiflexion and great toe extension. The response is a primitive reflex that disappears later in life. After 1 or 2 years of age, normal development of the central nervous system extinguishes this response.

In a positive Babinski response, upper motor neuron dysfunction disrupts the normal plantar cutaneous reflex and the primitive response re-emerges. It may take hours or days for these signs to emerge, as it is often absent in acute/hyperacute setting

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17
Q

What are causes of bradykinesia?

A
  • Parkinson’s disease
  • Dopamine antagonists – haloperidol, metoclopramide
  • Diffuse white matter disease – lacunar infarction(s)
  • Multisystem atrophy
  • Progressive supranuclear palsy
  • Corticobasilar degeneration
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18
Q

What is Broca’s aphasia?

A

Expressive aphasia, is a disorder of speech fluency (i.e. word production). Comprehension is less affected. Patients demonstrate speech that is laboured and short, lacks normal intonation, and is grammatically simple and monotonous.

Typically, phrase length is decreased and the number of nouns is out of proportion to the use of prepositions and articles

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19
Q

What is the mechanism behind broca’s aphasia?

A

Broca’s aphasia is typically caused by a lesion in the posterior inferior frontal gyrus of the dominant hemisphere.

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20
Q

Which artery is most commonly implicated in someone with Broca aphasia due to a stroke?

A

Most commonly branches of the superior division of the middle cerebral artery (MCA)

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21
Q

What speech abnormalities are seen in broca’s aphasia?

A
  • Nonfluent, mute or telegraphic spontaneous speech
  • Dysarthria
  • Impaired name recall
  • Impaired writing and reading
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22
Q

What associated features can be present with Broca’s aphasia, and why can they be present?

A

Associated contralateral motor and sensory findings are more commonly associated with Broca’s aphasia, due to the proximity of the motor cortex to the vascular distribution of the superior division of the middle cerebral artery

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23
Q

What is Brown-Sequard syndrome?

A

Rare clinical syndrome caused by spinal cord hemisection and is characterised by:

  • Ipsilateral
    • Below lesion - Weakness, Loss of light touch, vibration, proprioception and sensation below the lesion
    • Level of lesion narrow band of ipsilateral complete sensory loss
  • Contralateral
    • Below lesion - Loss of temperature and pain sensation
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24
Q

In brown-sequard syndrome, which spinal column tract is implicated in features of ipsilateral weakness and UMN signs?

A

Corticospinal tract lesion

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25
Q

In brown-sequard syndrome, which spinal column tract is implicated in features of ipsilateral loss of touch, vibration, proprioception below the lesion?

A

Dorsal column lesion

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26
Q

In brown-sequard syndrome, which spinal column tract is implicated in features of contralateral loss of pain and temperature below the level of the lesion?

A

Spinothalamic tract lesion

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27
Q

Why do those with Brown-Sequard syndrome develop contralateral loss of temp and pain sensation?

A

Lesion is above decussation at each spinal level, thus deficits are contralateral below the lesion

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28
Q

What can cause Brown-Sequard Syndrome?

A
  • Penetrating trauma
  • Multiple sclerosis
  • Mass lesion – tumour, abscess, AVM
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29
Q

What is cavernous sinus syndrome?

A

Clinical syndrome of multiple cranial nerve abnormalities affecting the contents of the cavernous sinus

  • Oculomotor nerve (CNIII)
  • Trochlear nerve (CNIV)
  • Ophthalmic division of the trigeminal nerve (CNV V1),
  • Maxillary division of the trigeminal nerve (CNV V2)
  • Abducens nerve (CNVI)
  • Sympathetic fibres
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30
Q

What are causes of cavernous sinus syndrome?

A
  • Septic thrombosis
  • Aseptic thrombosis
  • Cavernous carotid artery aneurysm
  • Mucormycosis
  • Pituitary apoplexy
  • Cavernous – carotid sinus fistula
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31
Q

What is the most common cause of cavernous sinus syndrome?

A

Septic thrombosis

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32
Q

What nerve in the cavernous sinus is first affected in cavernous carotid artery aneurysm?

A

Abducens - due to its close proximity to the cavernous segment of the internal carotid artery

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33
Q

What is clasp-knife rigidity?

A

Brisk relaxation of hypertonic muscle groups during tone assessment. The name arises from the similarity of the phenomenon to opening and closing the blade of a pocket knife due to the action of the spring.

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34
Q

What are causes of clasp-knife rigidity?

A

UMN lesions

  • Cerebral infarction
  • Cerebral haemorrhage
  • Cerebral palsy
  • Multiple sclerosis
  • Myelopathy
  • Mass lesion – tumour, abscess, AVM
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35
Q

What is clonus?

A

A rhythmic, sustained muscular contraction initiated with a brisk stretching force in a muscle group. Clonus is most commonly elicited in the ankle by abrupt passive dorsiflexion. It can also be assessed in other locations, such as the quadriceps, finger flexors, jaw and other muscle groups

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36
Q

What are causes of clonus?

A

UMN lesions

  • Cerebral infarction
  • Cerebral haemorrhage
  • Lacunar infarction, posterior limb internal capsule
  • Multiple sclerosis
  • Spinal cord injury
  • Mass lesion – tumour, abscess, AVM
  • Serotonin syndrome
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37
Q

What is thought to be the mechanism behind clonus?

A

Essentially it is a result of pronounced hyperreflexia. Clonus is caused by a self-sustaining, oscillating, monosynaptic stretch reflex.

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38
Q

What is the corneal reflex?

A

When the cornea is stimulated with a wisp of cotton, there is a reflexive blinking response in both eyes (a normal response)

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39
Q

What is dysarthria?

A

A disorder of speech articulation. Comprehension and speech content are not affected. There are several types of dysarthria that vary in the rate, volume, rhythm and sound of the patient’s speech

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40
Q

What are causes of dysarthria?

A
  • Intoxication (e.g. alcohol, benzodiazepine)
  • Drug toxicity (e.g. lithium, phenytoin)
  • Cerebellar infarction
  • Vertebral artery dissection
  • Cerebellar mass lesion – tumour, abscess, AVM
  • Multiple sclerosis
  • HSV cerebellitis
  • Hereditary cerebellar degeneration (Freidreich’s ataxia)
  • Paraneoplastic cerebellar degeneration
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41
Q

What is flaccid dysarthria?

A

Speech sounds slurred/nasal

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42
Q

What is spastic dysarthria?

A

Speech sounding as if patient is trying to squeeze words out of pursed mouth

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43
Q

What is ataxic dysarthria?

A

Speech is uncordinated - range, timing, direction innacurate, rate is slow and may be explosive

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44
Q

What is Hypokinetic dysarthria?

A

Speech may sound monotonous or slow-paced

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45
Q

What is hyperkinetic dysarthria?

A

Involuntary disruption in sounds +/- movements

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46
Q

What might cause an ataxic dysarthria?

A

Cerebellar dysfunction

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47
Q

What can cause spastic dysathria?

A

UMN lesions

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48
Q

What is dysdiadochokinesia?

A

https://www.youtube.com/watch?v=2EZqnmxWyAY

Dysdiadochokinesis is difficulty in performing rapid alternating movements. The patient’s movements may be slow and/or clumsy.

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49
Q

What are causes of dysdiadochokinesia?

A
  • Alcohol intoxication
  • Drug toxicity – lithium, phenytoin, benzodiazepine
  • Cerebellar infarction
  • Vertebral artery dissection
  • Cerebellar mass lesion – tumour, abscess, AVM
  • Multiple sclerosis
  • HSV cerebellitis
  • Hereditary cerebellar degeneration (Freidreich’s ataxia)
  • Paraneoplastic cerebellar degeneration
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50
Q

Why does dysdiadochokinesia occur?

A

Intermediate and lateral hemisphere dysfunction results in delays of motor initiation and movement termination at the end of movement (i.e. dysmetria). This, combined with abnormalities of movement force and acceleration, contribute to dysdiadochokinesia

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51
Q

What is essential tremor?

A

Essential tremor is a 4–12 Hz symmetric tremor of the upper limbs, with postural (seen in the outstretched arm) and/or kinetic (during movement) components. It may also affect the jaw, tongue, and head and neck muscles, leading to a characteristic ‘nodding yes’ or ‘shaking no’ tremor.

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52
Q

Why might you get a abnormal efferent corneal reflex in Bell’s Palsy?

A

Efferent corneal reflex defect (facial nerve)

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53
Q

Why might you get dry irritated eye in facial nerve palsy?

A
  • Orbicularis oculi muscle weakness results in incomplete eye closure
  • Lacrimal gland dysfunction
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54
Q

What are fasciculations?

A

Fasciculations are involuntary, nonrhythmic contractions of small muscle groups caused by spontaneous firing of motor units. They appear on the surface of the muscle as fine, rapid, flickering contractions, irregular in timing and location

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55
Q

What are causes of fasciulations?

A

Lower motor neuron sign

  • Benign fasciculations
  • Motor neuron disease (amyotrophic lateral sclerosis)
  • Radiculopathy
  • Depolarising paralytic agent – succinylcholine
  • Cholinergic toxicity – organophosphate toxicity
  • Funnel-web spider envenomation
  • Thyrotoxicosis
  • Poliomyelitis
  • Spinal muscular atrophy
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56
Q

What is thought to be the cause of fasciculations in LMN disorders?

A

Denervation and reinnervation of muscle fibres secondary to lower motor neuron disease causes the spontaneous excitation of individual motor units.

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57
Q

How does cholinergic toxicity cause fasciculations?

A

Due to potentiation of acetylcholine at the neuromuscular junction

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58
Q

What is the afferent limb of the gag reflex?

A

Glossopharyngeal nerve (CNIX)

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59
Q

What is the efferent limb of the gag reflex?

A

Glossopharyngeal and Vagus nerve

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60
Q

What is an abnormal gag reflex?

A

Absence of stylopharyngeus muscle and superior pharyngeal muscle constriction following stimulation of the posterior tongue and/or oropharynx. Absence of the gag reflex can be unilateral or bilateral.

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61
Q

What can cause a loss of gag reflex?

A
  • Normal variant
  • Generalised CNS depression
  • Glossopharyngeal nerve (CNIX) lesion
  • Vagus nerve (CNX) lesion
  • Lateral medullary syndrome (Wallenberg’s syndrome)
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62
Q

What is the glabellar tap sign?

A

Tapping the glabella (between the patient’s eyebrows) causes blinking, which typically ceases after several taps. Persistent blinking (i.e. more than 4 or 5 blinks) in response to glabellar tapping is abnormal (called Myerson’s sign).

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63
Q

What conditions can cause a positive glabellar tap sign?

A
  • Clasically - Parkinson’s disease
  • Alzheimer’s dementia
  • Vascular dementia
  • Frontotemporal dementia
  • Lewy Body dementia
  • Advanced HIV/AIDS dementia
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64
Q

What is global aphasia?

A

Global aphasia is a disturbance of speech with expressive and receptive components (i.e. a combination of Broca’s and Wernicke’s aphasia). Speech is nonfluent or nonexistent, and comprehension is impaired. Naming, repetition, reading and writing are all affected

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65
Q

What are causes of global aphasia?

A
  • Cerebral infarction, MCA territory
  • Cerebral haemorrhage
  • Alzheimer’s disease
  • Vascular dementia
  • Mass lesion – tumour, abscess, AVM
  • Primary progressive aphasia
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66
Q

What are features of global aphasia?

A
  • All aspects of speech impaired
  • Contralateral motor/sensory signs
  • Contralateral hemianopia
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67
Q

What’s the most common cause of global aphasia?

A

MCA territory infarct

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68
Q

What is the grasp reflex?

A

The patient involuntarily grasps the examiner’s fingers when the examiner strokes the patient’s thenar eminence. The grasp reflex is a primitive reflex present in infancy, which normally disappears later in life

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69
Q

What are causes of a positive grasp reflex?

A
  • Alzheimer’s dementia
  • Vascular dementia
  • Frontotemporal dementia
  • Lewy body dementia (LBD)
  • Advanced HIV/AIDS
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70
Q

Why is hand dominance important?

A

Hand dominance is clinically significant in the context of dominant cortical localising signs. The side of hand dominance correlates with the side of the dominant cerebral hemisphere and therefore has potential localising value.

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71
Q

What is hemineglect syndrome?

A

A disorder of conscious perception, characterised by a lack of awareness of the contralateral visual hemispace and contralateral body. The patient may be completely unaware of their own body or objects in the neglected space (i.e. anosognosia). The presence of hemineglect is typically evaluated with clock face drawing, search/cancellation and/or line bisection tests.

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72
Q

What is sensory neglect?

A

Patient ignores visual, tactile or auditory stimuli in the contralateral hemispace

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73
Q

What is motor neglect?

A

Patient performs fewer movements in the contralateral hemispace

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74
Q

What is conceptual neglect?

A

Patient’s internal representation of own body and/or external environment exhibits neglect

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75
Q

What are causes of hemineglect syndromes?

A
  • Cerebral infarction/haemorrhage
  • Mass lesion - Tumour, Abscess, AVM
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76
Q

What is the most common lesion site in someone with a hemineglect syndrome?

A

Temporoparietal junction of non-dominant hemisphere - mediate conscious representation of sensation, motor activities such as visual scanning and limb exploration, and motivational relevance

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77
Q

What is a high stepping gait?

A

A high stepping gait is characterised by pronounced hip and knee flexion, in order to clear the lower limb or limb(s) with foot drop during leg swing

78
Q

What can cause a high-stepping gait?

A
  • Common peroneal nerve neuropathy
  • L5 radiculopathy
  • Sciatic nerve palsy
  • Length-dependent peripheral neuropathy – alcohol, diabetes mellitus
  • Hereditary peripheral neuropathy – Marie–Charcot–Tooth disease
  • Myopathy – scapuloperoneal muscular dystrophy
79
Q

What is the mechanism foot drop?

A

Caused by weakness of the anterior compartment muscles of the leg (e.g. tibialis anterior, extensor hallicus longus, extensor hallicus brevis muscles).

80
Q

What is hyperreflexia?

A

Stretch reflexes are more brisk than normal. Hyperreflexia is an upper motor neuron sign.

81
Q

What are causes of hyperreflexia?

A
  • Normal variant
  • Cerebral infarction, MCA territory
  • Cerebral haemorrhage
  • Lacunar infarction, posterior limb internal capsule
  • Multiple sclerosis
  • Spinal cord injury
  • Brainstem lesion (medial medullary syndrome)
  • CNS mass lesion – tumour, abscess, AVM
  • Serotonin syndrome
  • Clostridium tetani infection (tetanus)
82
Q

What side does hyperreflexia occur on in upper motor neuron lesions?

A
  • Contralateral side - if lesion present above decussation
  • Ipsilateral - if below decussation
83
Q

Where do the motor fibres deccusate in the brain?

A

Anterior median fissure of the medulla oblongata as the pyramidal decussation or motor decussation

84
Q

What is hyporeflexia?

A

Stretch reflexes are decreased (hyporeflexia) or absent (areflexia) despite reinforcement manoeuvres (e.g. Jendrassik manoeuvre).

85
Q

What are causes of hyporeflexia?

A

Lower motor neuron signs

  • Hyperacute UMN disorder – CVA, spinal cord injury
  • Radiculopathy – intervertebral disc herniation, spondylosis
  • Peripheral neuropathy
  • Myasthenia gravis
  • Guillain–Barré syndrome
  • Poliomyelitis
  • Botulism
  • Tick paralysis
86
Q

What is hypotonia?

A

Decreased resistance to passive movement due to decreased resting muscle tone. The limb may feel ‘floppy’, the outstretched arm when tapped may demonstrate wider than normal excursions, and the knee jerk may be abnormally pendular

87
Q

What are causes of hypotonia?

A

Lower motor neuron

  • Peripheral neuropathy
  • Myasthenia gravis
  • Guillain–Barré syndrome
  • Poliomyelitis
  • Botulism
  • Tick paralysis
88
Q

What happens to tone in cerebellar disorders?

A

Hypotonia - mechanism not known

89
Q

What is an intention tremor?

A

Intention tremor is a slow (2–4 Hz) tremor during voluntary movement that develops as the limb approaches the target.

90
Q

What tests would you do to assess for an intention tremor?

A
  • Finger-to-nose test
  • Heel-shin sign
91
Q

Why does an intention tremor occur?

A

Delays in motor initiation and movement termination, and abnormalities of movement force and acceleration, contribute to intention tremor

92
Q

What can cause an intention tremor?

A
  • Intoxication – alcohol, benzodiazepine
  • Cerebellar infarction
  • Multiple sclerosis
  • Vertebral artery dissection
  • Cerebellar mass lesion – tumour, abscess, AVM
  • HSV cerebellitis
  • Hereditary cerebellar degeneration (Freidreich’s ataxia)
  • Paraneoplastic cerebellar degeneration
93
Q

What is a positive jaw jerk reflex?

A

Brisk reflex - sign of upper motor neuron lesion above the pons

94
Q

What are causes of first order sympathetic neuron lesions which can lead to the development of horners syndrome?

A
  • Hypothalamic lesions (e.g. infarct, tumour),
  • Lateral medullary syndrome (Wallenberg’s syndrome)
  • Syringomyelia
95
Q

If someone presented with the following; 1) what else would you look for and 2) what would be the clinical syndrome present?

A
  1. Anhidrosis
  2. Right horner’s syndrome - Ptosis with apparent enopthalmous, miosis
96
Q

What are causes of second-order sympathetic neuron lesions which can lead to the development of horner’s syndrome?

A
  • Thoracic aortic aneurysm
  • Lower brachial plexus injury (e.g. Klumpke’s palsy)
  • Pancoast’s tumour
  • Carotid artery dissection
  • Iatrogenic injury following carotid endarterectomy
97
Q

What are examples of third order sympathetic neuron lesions that cause horner’s syndrome?

A
  • Head and neck trauma
  • Local eye pathology
98
Q

What is the course of the third order sympathetic neuron involved in horner’s syndrome?

A

From the cervical ganglion at the level of C2 to the pupillary dilator muscle and the superior tarsal muscle

99
Q

What is the course of the first order sympathetic neuron involved in horner’s syndrome?

A

From the hypothalamus to the C8–T1 level of the spinal cord.

100
Q

What is myotonia?

A

Percussion myotonia is a sustained muscle contraction following percussion of a muscle. Grip myotonia is a sustained muscle contraction following forceful contraction of the hand muscles

101
Q

What are causes of a brisk jaw jerk reflex?

A
  • Normal variant
  • Diffuse white matter disease – lacunar infarction(s)
  • Vascular dementia
  • Motor neuron disease (amyotrophic lateral sclerosis)
  • Bilateral cerebral infarction
  • Multiple sclerosis
  • Progressive multifocal leucoencephalopathy (PML)
  • Central pontine myelinolysis
102
Q

What is a brisk jaw jerk reflex a sign of?

A

Bilateral upper motor neuron disease above the pons - Loss of supranuclear innervation of the motor trigeminal nucleus causes hyperexcitability of alpha motor neurons innervating the masseter muscles

103
Q

What afferent and efferent nerve is involved in the aw jerk reflex?

A

Mandibular branch of the trigeminal nerve

104
Q

What are causes of enhanced phsyiological tremor?

A
  • Hyperthyroidism
  • Hypoglycaemia
  • Withdrawal states
  • Sympathomimetic agents
  • Fatigue
  • Anxiety
  • Fear
105
Q

What is the physiology behind an enhanced physiological tremor?

A

Caused by increases in circulating catecholamines (e.g. adrenaline, noradrenaline) and/or catecholamine receptor upregulation (e.g. hyperthyroidism), which increase the twitch force of motor units

106
Q

What is pronator drift?

A

https://www.youtube.com/watch?v=o8zkr3tmszQ

There is asymmetric pronation and downward arm drift when the patient is instructed to extend both arms with palms straight facing the ceiling.

Downward arm drift, forearm pronation and flexion of the wrist and elbow typically begin distally and progress proximally

107
Q

What is pronator drift generally a sign of?

A

Upper motor neuron lesion - contralateral cerebral hemisphere

108
Q

What are causes of pronator drift?

A
  • Cerebral infarction, MCA territory
  • Lacunar infarction, posterior limb internal capsule
  • Cerebral haemorrhage, parenchymal
  • Mass lesion – tumour, abscess, AVM
  • Subdural haematoma
109
Q

What is the mechanism behind pronator drift?

A

When visual cues are removed, subtle upper motor neuron weakness causes the weak upper limb to pronate and drift downwards.

110
Q

What is rigidity?

A

Increased resistance to passive movement due to an abnormal increase in resting muscle tone.

111
Q

What are the three characteristic features of rigidity?

A
  • Magnitude of resistance during passive movement is the same with slow or fast movement
  • Equal flexor and extensor tone
  • No associated weakness.
112
Q

What is rigidity a sign of?

A

Sign of extrapyramidal disease

113
Q

What conditions is rigiditiy associated with?

A
  • Parkinson’s disease
  • Dopamine antagonists – haloperidol, metoclopramide
  • Diffuse white matter disease – lacunar infarction(s)
  • Multisystem atrophy
  • Progressive supranuclear palsy
  • Corticobasilar degeneration
114
Q

What are causes of a positive romberg’s test?

A

Common

  • Intoxication – alcohol, benzodiazepine
  • Vestibulotoxic drugs – furosemide, gentamicin

Uncommon

  • Subacute combined degeneration of the cord (Vitamin B12 deficiency)
  • Tabes dorsalis (tertiary syphilis)
  • Vestibular neuritis
115
Q

What is the mechanism behind a positive romberg’s test?

A

A positive Romberg test is caused by:

  • Proprioceptive dysfunction - peripheral neuropathy, dorsal column dysfunction
  • Vestibular dysfunction - vestibular neuritis

Both of these causes are sensory in nature, so a positive Romberg’s test indicates a sensory ataxia

116
Q

What tract carries sensory information from light touch, vibration and proprioception?

A

Dorsal column tract and medial lemniscus pathway

117
Q

What might give the following sensory loss?

A
  • MCA territory infarction
  • Mass lesion, sensory cortex
118
Q

What might give the following diostribution of sensory loss?

A
  • Mass lesion, sensory cortex
  • ACA territory infarction
119
Q

What might give you the following sensory loss distibution?

A
  • Thalamic lesion
  • Anterior limb, internal capsule lesion
  • ICA (ACA + MCA) territory infarction
120
Q

What might give you the following sensory loss distribution?

A

Lateral medullary syndrome (Wallenberg’s syndrome)

121
Q

What might give you loss of pain and temperature in both arms in the following (cape) distribution?

A

Central cord syndrome - cervical spinal cord

122
Q

What might the following sensory loss distribution be caused by?

A

Cervical spinal cord lesion

123
Q

What might the following sensory loss distribution be caused by?

A

Spinal cord lesion below T1, above L1/L2

124
Q

What might sensory loss in the following distribution indicatea as a cause?

A

Glove and stocking distribution

Length-dependent peripheral neuropathy e.g. diabetic neuropathy

125
Q

What might cause sensory loss?

A

Common

  • Compression mononeuropathy – carpal tunnel syndrome
  • Peripheral neuropathy – diabetic neuropathy
  • Cerebral infarction
  • Cerebral haemorrhage
  • Spinal cord injury
  • Radiculopathy

Less common

  • Transverse myelitis
  • Lateral medullary syndrome (Wallenberg’s syndrome)
  • Compartment syndrome
  • Syringomyelia
  • Mass lesion – tumour, abscess, AVM
126
Q

What do sensory cortex lesions cause in terms of sensory loss?

A

Contralateral complete hemisensory loss in the distribution of structures of the sensory homunculus

127
Q

What would an anterior limb, internal capsule lesion cause in terms of sensory loss?

A

Pure contralateral complete hemisensory loss of the face, arm and leg due to the dense distribution of sensory fibres in this region

128
Q

What do brainstem lesions cause?

A

Characterised by:

  • Contralateral sensory and/or motor deficits
  • Ipsilateral cranial nerve motor/snesory deficits
  • Contralateral hyperreflexia
  • Contralateral spastic weakness
  • Ipsilateral ataxia
129
Q

What does radiculopathy cause in terms of clinical signs?

A

Positive and negative features in distribution fo dermatome

  • Positive
    • Dysaesthesia or burning
    • Paraesthesias
    • Pain
  • Negative
    • Anaesthesia or numbness
130
Q

What are causes of length-dependent neuropathy?

A
  • Diabetes
  • Alcohol
  • Inherited neuropathies
  • Heavy metal toxicity
131
Q

What is spasticity?

A

Spasticity is increased resistance to passive movement due to an abnormal increase in resting muscle tone

132
Q

What are the three distinct features of spasticity?

A
  1. Muscle tone increases with the velocity of passive movement
  2. Flexor–extensor tone dissociation - increased tone in flexors of the arms and extensors of the lower limbs
  3. Weakness is present.
133
Q

What is spasticity indicative of?

A

UMN lesion

134
Q

Why do upper motor neuron lesions cause spasticity?

A

Causes a decrease in inhibitory interneuron activity and an increase in gamma motor neuron activity, resulting in a state of hyperexcitability of alpha motor neurons.

Hyperexcitability of alpha neurons results in increased resting muscle tone and increased resistance during passive movement.

135
Q

What would weakness in turning the head left indicate?

A

Right sternocleidomastoid weakness

136
Q

What would weakness in turning the head right indicate?

A

Left sternocleidomastoid weakness

137
Q

What are causes of accessory nerve palsy?

A

Peripheral nerve lesions secondary to trauma or mass lesions.

  • Complicaiton of neck dissection
  • Penetrating trauma of posterior triangle
  • Mass lesion - tumour, abscess, AVM
138
Q

What would cause the following?

A

Left Hypoglossal nerve palsy

139
Q

What side is the lesion which causes the following deformity?

A

Left

140
Q

What are causes of the following?

A
  • Iatrogenic – complication of carotid endarterectomy
  • Penetrating neck trauma
  • Carotid artery aneurysm
  • Hypoglossal canal stenosis
  • Mass lesion – tumour, abscess
  • Carotid artery dissection
141
Q

Why does the following occur in hypoglossal nerve palsy?

A

If genioglossus (supplied by hypoglossal nerve) weakness is present, the tongue deviates towards the side of weakness, due to loss of the medial force on the affected side

142
Q

What are the characteristic findings in trochlear nerve palsy?

A
  • Hypertropia (upward deviation)
  • Extorsion (external rotation)
  • Head tilt, in the direction opposite to the side of the affected eye.
143
Q

What is truncal ataxia?

A

Postural instability due to incoordination of the proximal muscles groups of the body assessed while sitting upright and/or oscillatory movements of head and neck (i.e. titubation). Patients may require assistance to maintain an upright posture.

144
Q

What are causes of truncal ataxia?

A
  • Alcohol intoxication
  • Drug toxicity – lithium, phenytoin, benzodiazepine
  • Cerebellar infarction
  • Basilar artery territory infarction
  • Multiple sclerosis
  • Mass – tumour, abscess, AVM
  • HSV cerebellitis
  • Hereditary cerebellar degeneration (Freidreich’s ataxia)
  • Paraneoplastic cerebellar degeneration
145
Q

Damage to what structures in the cerebellum cause truncal ataxia?

A

Vermis and flocculonodular lobe

146
Q

What is uvular deviation?

A

When a patient says ‘ah’, there is dynamic deviation of the uvula to one side upon contraction of the palator constrictor muscle.

147
Q

Lesions in what nerves cause uvular deviation?

A
  • Nucleus ambiguus lesion
  • Glossopharyngeal nerve (CNIX)
  • Glossopharyngeal nerve (CNIX) and vagus nerve (CNX) palsies.
148
Q

What are common causes of uvular deviation?

A
  • Diabetic mononeuropathy/microvascular infarction
  • Iatrogenic – complication of tonsillectomy
  • Lateral medullary syndrome (Wallenberg’s syndrome)
  • Cerebellopontine tumour
  • Internal carotid artery dissection
  • Mass – glomus tumour, AVM
  • Trauma – jugular foramen fracture
149
Q

What side does the uvula deviate in glossopharyngeal/vagus nerve palsy?

A

Away from affected side

150
Q

What is vertical gaze palsy?

A

Vertical gaze palsy is a group of uncommon gaze disorders that include upward gaze palsy, downward gaze palsy and a combined upward and downward gaze palsy

151
Q

What is upward gaze paresis caused by?

A

Posterior commissure lesion

152
Q

What is a downward gaze paresis caused by?

A

Bilateral rostral interstitial medial longitudinal fasciculus (riMLF)

153
Q

What are causes of vertical gaze palsies?

A
  • Pinealoma
  • Hydrocephalus
  • Progressive supranuclear palsy (PSP)
  • Multiple sclerosis
  • Wernicke’s encephalopathy
  • Tay–Sachs disease
  • HIV/AIDS encephalopathy
154
Q

What can cause the following pattern of muscle weakness?

A
  • Contralateral motor cortex lesion
  • Ipsilateral cervical spinal cord lesion
  • Contralateral posterior limb, internal capsule lesion
  • Todd’s paralysis
155
Q

What are causes of the following pattern of muscle weakness?

A
  • Guillain–Barré syndrome
  • Tick paralysis
156
Q

What can cause the following distribution of muscle weakness?

A
  • Botulism
  • Miller Fisher variant Guillain–Barré syndrome
  • Diphtheria polyneuropathy
157
Q

What can cause the following pattern of weakness?

A
  • Complete cervical spinal cord lesion
  • Anterior cord syndrome
158
Q

What can cause the following distribution of muscle weakness?

A
  • Cervical syringomyelia
  • Cervical radiculopathy
159
Q

What can cause the following pattern of muscle weakness?

A
  • Peripheral neuropathy
  • Myotonic dystrophy
160
Q

What can cause the following distribution of muscle weakness?

A

MCA territory infarction

161
Q

What can cause the following distribution of muscle weakness?

A
  • Posterior limb, internal capsule lesion
  • ICA territory (ACA + MCA) infarction
162
Q

What can cause the following pattern of muscle weakness?

A

Brainstem lesion

163
Q

What can cause the following distribution of muscle weakness?

A

Myopathy

164
Q

What areas are supplied by the anterior cerebral artery?

A
  • Medial aspects of the frontal and parietal lobes
  • Basal ganglia
  • Anterior fornix
  • Anterior corpus callosum - motor, cognitive, sensory
165
Q

What area does the middle cerebral artery supply?

A
  • Lateral aspects of frontal, temporal and parietal lobes
  • Corona radiata
  • Globus pallidus
  • Caudate and putamen
166
Q

What area does the posterior cerebral artery supply?

A
  • Occipital lobe
  • Inferomedial temporal lobe
  • Large portion of the thalamus
  • Upper brainstem and midbrain
167
Q

What a upper motor neuron lesion signs?

A
  • Spasticity - velocity dependent increase in tone
  • Clonus
  • Weakness
  • Hyperreflexia
  • Babinski sign
168
Q

What is a pyramidal pattern of muscle weakness?

A

Corticospinal tracts

  • Arm - extensors predominatly affected
  • Legs - flexors are predominantly affected
169
Q

What are lower motor neuron signs?

A
  • Fasciculations
  • Muscle atrophy
  • Hypotonia
  • Weakness
  • Hyporeflexia/areflexia
170
Q

What is the difference between pyramidal and extra-pyramidal signs?

A

Extrapyramidal signs and symptoms occur as a result of pathology in the basal ganglia. Pyramidal signs occur following an upper motor neurone lesion.

171
Q

What is Wernicke’s Aphasia?

A

Receptive aphasia is a disorder of language comprehension. Speech fluency (word production) is typically not affected. The patient’s speech is meaningless or strange and may contain paraphasic errors (inappropriate word substitutions based on meaning or sound

172
Q

What features of speech are impaired in Wernicke’s Aphasia?

A
  • Naming
  • Comprehension
  • Repetition
  • Reading
173
Q

What can cause Wernicke’s Aphasia?

A
  • MCA territory infarction
  • Cerebral haemorrhage
  • Vascular dementia
  • Migraine (transient)
  • Alzheimer’s disease
  • Mass lesion – tumour, abscess, AVM
  • Primary progressive aphasia
174
Q

What is the mechanism behind Wernicke’s Aphasia?

A

Caused by a lesion in the posterior superior temporal gyrus of the dominant hemisphere supplied by MCA.

175
Q

What does occlusion of the anterior cerebral artery cause in terms of clinical signs?

A
  • Contralateral leg +/- similar/milder arm features
  • Spared face
176
Q

What can occlusion of the middle cerebral artery cause in terms of clinical signs?

A
  • Contralateral hemiparesis
  • Hemisensory loss - esp face and arm (look at homunculus)
  • Contralateral homonymous hemianopia - optic radiation involvement
  • Dysphasia - dominant hemisphere
  • Visuospatial disturbance - non-dominant hemisphere
177
Q

What can occlusion of the posterior cerebral artery cause in terms of clinical signs?

A
  • Contralateral homonymous hemianopia
178
Q

What does occlusion of the vertebrobasilar system cause in terms of clinical signs?

A

Cerebellum, brainstem, occipital lobes:

  • Hemianopia
  • Cortical blindness
  • Diplopia
  • Nystagmus
  • Ataxia
  • Dysarthria
  • Dysphasia
  • Hemi/qudraplegia
  • Unilateral/bilateral sneory symptoms
179
Q

What syndromes can occur due to brainstem infarction?

A
  • Lateral meduallry syndrome
  • Locked-in syndrome
180
Q

What is L’hermittes Phenomenon?

A

An electrical sensation that runs down the back and into the limbs on neck flexion. The sensation can feel like it goes up or down the spine

181
Q

What is the mechanism behind L’hermittes phenomenon?

A

Suggests a lesion or compression of the upper cervical spinal cord or lower brainstem—usually dorsal columns of the cervical cord or caudal medulla.

182
Q

What are causes of L’Hermittes Phenomenon?

A
  • MS
  • Transverse myelitis
  • Cervical myelopathy
  • Radiation myelopathy
  • Vitamin B12 deficiency (subacute combined degeneration)
  • Compression of the spinal cord in the neck from any cause - cervical spondylosis, disc herniation, tumor, and Arnold-Chiari malformation, trauma
183
Q

What is the doll’s eye reflex?

A

Vestibulo-ocular reflex

Passive head turning produces conjugate ocular deviation away from the direction of rotation

https://www.youtube.com/watch?v=B8SXlFeyNLM

184
Q

What would indicate a positive doll’s eye reflex?

A

Eyes move conjugately away from the side that the head is moving towards

185
Q

What would indicate a negative Doll’s eye reflex?

A

Eyes fixed midorbit on movement

186
Q

What are causes of absent doll’s eye reflex?

A
  • Deep coma
  • Brainstem lesion
  • Brain death
187
Q

What are features of a disorder in the basal ganglia?

A

Extrapyramidal symptoms/signs:

  • Akinesia/bradykinesia
  • Rigidity
  • Tremor
  • Dyskinesia
  • Dystonia
188
Q

What is the extrapyramidal system?

A

part of the motor system network causing involuntary actions. The system is distinguished from the tracts of the motor cortex that reach their targets by traveling through the pyramids of the medulla. The pyramidal tracts (corticospinal tract and corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers on the modulation and regulation (indirect control) of anterior (ventral) horn cells.

189
Q

How does the extra-pyramidal system differ from the pyramidal system in terms of motor control?

A

Pyramidal is involved in voluntary motor control of muscles. Extrapyramidal target lower motor neurons in the spinal cord that are involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex

190
Q

What are extrapyramidal symptoms?

A

Collection of movement disorders that are typically seen due to disruption of pathways in basal ganglia:

  • Bradykinesia
  • Rigidity
  • Athetosis
  • Chorea
  • Ballismus
  • Tics
  • Tremors

Neurology (34 decks)

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