Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 > Neuro > Flashcards

Neuro Flashcards

1
Q

What is weakness

A

objective loss of muscle strength (formally tested)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Recording muscle strength

A

5 normal
4 moves against resistance but can be overcome
3 moves against gravity but not resistance
2 moves only when positioned to eliminate gravity
1 flicker of movement
0 complete paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

UMN signs

A

normal bulk
Increased tone (velocity dependent)
Brisk reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

localizing UMN weakness to the cortex

A

Aphasia (L hemisphere)
Spatial neglect (R hemisphere)
Face and arm>leg weakness - lateral motor cortex
Opposite - medial motor cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Localizing UMN weakness to the parietal cortex

A

Normal somatic and decreased cortical sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

localizing UMN weakness to spinal cord

A

Presence of a sensory level, and sphincter disturbance
Above T1= arm and leg
Below T1= leg only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Localizing UMN weakness to the brainstem

A

Cranial nerve involvement
Above facial nucleus (pons) = F, A & L equal
Lower pons/medulla = A & L equal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Weakness in myasthenia

A

variable with abnormal fatiguability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Onset pattern of myasthenia gravis

A

Ocular 65% (50% have AChR +ve Ab)
Bulbar 10%
Leg 10%
Generalized 10% (80% +ve Ab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Differentials with proximal LMN weakness

A

subacute myopathy, chronic myopathy, myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Differentials with distal LMN weakness

A

Motor neuron disease, motor multifocal neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Differentials LMN weakness with atrophy

A

chronic myopathy (proximal)
Motor neuron disease (distal)
Late motor multifocal neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Differentials LMN weakness without atropjy

A

Subacute myopathy
Myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Differentials LMN weakness with ptosis

A

Myasthenia gravis
Mitochondrial chronic myopathy
Rarely in subacute myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Differentials in LMN weakness with diplopia

A

Myasthenia gravis
Rarely in chronic myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CK in subacute myopathy

A

Very high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CK in chronic myopathy

A

Normal-mildly elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

CK in motor neuron disease

A

Normal-mildly elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CK in myasthenia

A

Usually normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mean age of onset in MND

A

65, but quite variable, and variable onset pattern. Median survial’ is 30 months from symptoms onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Symptoms of MND

A

Progressive painless weakness
UMN: Weakness, spasticity, brisk reflex, planters up
LMN: Weakness, wasting, fasciculation
No sensory or sphincter dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Acute phase features of UMN localisation

A

generally hypotonia
Low/absent reflexes
Plantar responses extensor or mute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Chronic phase features of UMN localisation

A

clasp-knife (velocity dependent) increased tone
Brisk reflexes
Extensor plantar responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Acute phase features of LMN localisation

A

no atrophy
Normal/reduced tone
Low/absent reflexes
Flexor plantar response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Chronic phase features of LMN localisation

A

atrophy
Reduced tone
Reduced/absent reflexes
Flexor plantar responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Localizing UMN weakness to the subcortical white matter

A

equal weakness of F, A & L = hemiparesis )
- posterior limn of internal capsule
Hemisensory change - thalamus
Parkinsonism - basal ganglia
Homonymous hemianopia - optic radiations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Anterior horn motor neuron syndromes distribution of weakness

A

pure LMN pattern of weakness
Can affect any limb, possible distal wasting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Additional features of Anterior horn motor neuron syndromes

A

fasciculations
Bulbar symptoms (dysphagia, dysarthria), tongue wasting
Respiratory failure may feature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Anterior horn motor neuron syndromes possible causes

A

spinal muscular atrophy
Early stages of amylotrophic lateral sclerosis
Acute flaccid myelitis (eg. Viral, polio and west Nile virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Multifocal motor neuropathy

A

onset can be indistinguishable from anterior horn syndromes.
Typically distal predominant weakness with late wasting, preference for upper limbs eg fingers, less bulbar.
Immune so treat w IV Ig or plasma exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Distribution of weakness in NMJ disease

A

typically proximal
Fluctuating and worse towards end of day
Fatiguable
Ptosis and complex ophthalmoplegia, and dysarthria and dysphagia common
Typically no atrophy unless disuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Lambert Eaton myasthenic syndrome features

A

Repeated muscle contractions lead to increased muscle strength
Limb girdle weakness (lower limb first)
Hyporeflexia
Autonomic sympt (dry mouth, importance, difficult micturatikn)
Not commonly eye issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Labert Eaton Myasthenic Syndrome EMG and Ab

A

Incremental response to repetitive electrical stimulation and Ab to Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

treatment of Lambert Eaton Myasthenic Syndrome

A

Treatment of underlying cancer
Immunosuppression eg w pred
Trials of 3;4-diaminopyridine via blocking K channel efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Brown Sequard syndrome tracts affected and clin feat

A

Lateral corticospinal tract
Dorsal columns
Lateral spinothalamic tract

Ipsilateral spastic paresis below lesion
Ipsilateral loss of proprioception and vibration sensation
Contralateral loss of pain and temperature sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Subacute combined degeneration of the spinal cord

A

caused by vitamin B12 and E deficiency.
Tracts: Lateral corticospinal, dorsal columns and spinocerebellar tracst
Feat
Bilateral spastic paresis
Bilateral loss of proprioception and vibration sensation
Bilateral limb ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Friedrich’s ataxia

A

Tracts: Lateral corticospinal, dorsal columns and spinocerebellar tracst
Feat
Bilateral spastic paresis
Bilateral loss of proprioception and vibration sensation
Bilateral limb ataxia
Cerebellar ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Anterior spinal artery occlusion tracts and feat

A

lateral corticospinal tracts
Lateral spinothalamic tracts

Feat
Bilateral spastic paresis
Bilateral loss of pain and temp sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

syringomyelia

A

tracts: Ventral horns
Lateral spinothalamic tract

Feat
Flaccid paralysis (typical intrinsic hand muscles)
Loss of pain and temp sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Neurosyphilis (tabes dorsalis)

A

affect dorsal columns
Lose proprioception and vibration sensarion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Botulism

A

a possible cause for NMJ disease
Infection from neuroparalytic toxin, rare in West although can be from home canned food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MND pure upper and pure lower forms

A

Pure UMN degeneration - primary lateral sclerosis
Pure LMN: Progressive muscular atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cervical myeloradiculopathy

A

Usually follows cervical/spinal trauma
Progression halts after some time
LMN finding usually solely cervical/upper thoracic region plus UMN signs in lower limbs
MRI myelopahty and multiple nerve root involvement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Numbness (hypoaesthesia)

A

decreased sensitivity to, or diminution of sensory perception in any modality. Most often referred to as pain (hypoalgesia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

tingling (paraesthesia)

A

abnormal, not painful, sensation that can be pins and needles, crawling, or electric sensatkk s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Dysaesthesia

A

Abnormal, painful sensations, usually burning or electric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Guillain-Barré presentaiton

A

occurs at any age but more common in elderly and M>F
2/3 have preceding infection most commonly respiratory. Campylobacter jej = worse prognosis
Progression of symptoms over days to 4 weeks - legs symmetrically weaker than arms, mild sensory symptoms, CN involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ix for GBS

A

Elevated CSF protein with fewer than 10 cells
EMG/NCV: Conduction block, incr distal latency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Radiculopathies

A

Sensation loss in 1 nerve root territory
Pain nerve root irritation, can be provoked on exam
Often one reflex lost
Frequently structural, eg disc compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Plexopathies

A

> 1 nerve root territory affected
Pain spontaneous or absent, can rarely be triggered
Often >1 reflex lost
Cause can be structural (eg tumours), or post radiation, or inflammatory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Mononeuropathies

A

Lesion of a single peripheral merge, most commonly due to compression or trauma
Weakness and later wasti g in muscles innervated by said nerve, and numbness in same territory
Reflexes only affected if innervated myotomes are involved in motor response of reflex arc
Abnormal posturing of affected limb due to selective weakness pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Median mononeuropathy

A

sensory loss over Palmar side of fingers 1 to 3, and radial side of 4. Thenar atrophy
Mostly due to carpal tunnel
Phalen sign: Tingling in median nerve territory by forced flexion of wrist
Tinnel sign: Tapping on nerve can provoke abnormal sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Mononeuritis multiplex fearures

A

sequential or simultaneous sensory change and weakness in different peripheral nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Dangerous causes of mononeuritis multiplex

A

systemic vasculitis (especially when painful)
Diabetes mellitus
Infection eg HIV and leprosy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Length dependent peripheral neuropathy features

A

Sensory alteration in distal lower limn ascending to knee, at which point symptoms mat be experienced in fingers and hands (glove and stocking)
Predominantly distal weakness with early loss of ankle reclexese with ascension up limb as disease progresses. Proximal muscle strength only affected in extreme cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Causes of length dependent peripheral neuropathy

A

Toxic-metabolic - artic diabetes mellitus, also B12/folste deficiency, thyroid dysfunction, liver/kidney derangements
Inherited = Charcot Marie Tooth: With high arched feet, absence of positive sensory symptoms (paraesthesia) but numbness distally and positive FHx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Non-parkinsonian hypomobile patient differentials

A

severe depression
Hypothyroidism
Toxic or metabolic encephalopathies
Ankylosing spondylitis
Cautious gate (eg past vestibulR neuritis)
Senile gate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Red flags for atypical parkinsonism

A

supranuclear gaze palsy
Cerebellar ataxia
Early falls
Early orthostatic hypotension
Early incontinence
Poor response to L Dopa
Gait apraxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Myoclonus definition

A

Brief, shock like, involuntary movements caused by muscular contractions or inhibituons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

dystonia definition

A

Sustained or intermittent muscle contractions causing abnormal, often repetitive movements, postures, or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Chorea definition

A

Involuntary brief, random, irregular contractions flowing from one body part to another and giving, in less severe cases, an appearance if fidgetiness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Tic disorders definition

A

Tics are repeated, individually recognizable, intermittent movements or movement fragments that are almost always briefly suppressible, and are usually associated with awareness of an urge to perform the movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Degenerative causes of parkinsonism

A

Parkinsons disease
Lewy body dementia
Atypical: Multisystem atropjy, progressive supranuclear palsy, corticobasal syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Secondary causes of parkinsonism

A

Drugs eg antipsychotics
Toxins or heavy metals
Vascular
Infections or other brain insults
Structural lesions (tumour)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

symptoms of PD

A

Tremor
Rigidity
Akinesia
Postural instability
Hypomimia
Hypophonia
Micrographia
Dribbling
Bent spind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Non motor fearures of PD

A

Anosmia
Constipation
REM sleep behaviour disorder
Anxiety/depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Other dysautonomic featurea of PD

A

ortostatic hypotension
Urinary dysfunction
Erectile dysfunciton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Cognitive impairment in pd

A

dementia often accompanied by visual hallucinations
Cognitive fluctuations with minutes to hours of drowsiness, slurred speech and cognitive slowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Aetiology progressive supranuclear palsy

A

Rare degenerative disorder of about 5/100000
Mean onset age 63.
M>F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

clinical features of PSP

A

Symmetrical parkinsonism with prominent axial rigidity
A “worried” or “surprised”facial appearance with prominent frowning
Problems with downgaze are an early feature
Frequent dementia and with frontal features, eg apathy and or disinhibitin
commonly urinary incontinence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Pathology of PSP

A

Accumulation of tau protein, rather than of alpha synuclein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Multisystem atrophy aetiology

A

rare degenerative, prevalence 4.4/100000.
Peak age of onset 55 to 60
M and F roughly equal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Clinical features of MSA

A

Parkinsonian syndrome with prominent early autonomic failure with orthostatic hypotension, urinary dysfunction and constipation
Cerebellar dysfunction can develop or be present from outset
Respiratory abnormalities during sleep assoc w poor prognosis (strifor and prominent sleep apnoea)
REM sleep behaviour disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Pathology of MSA

A

Accumulation of alpha synuclein in the brain, but unlike in PD, there are no Lewy bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Corticobasal syndrome prefalence

A

rare neurodegenerative disorder w prevalence 4.4-7.3 per 100,000
Age of onset typically 50 to 70
F slightly more than M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Clinical features of corticobasal syndrome

A

Strikingly asymmetrical parkinsonism of the upper limbs
Early prominent loss of hand dexterity, and jerks or tremor common
Neuro exam finds:
Apraxia (incapable of imitating gestures)
Myoclonus (triggered by stimulating fingers or hand)
Dystonia (abnormal posturing of hand and fingerz)
Alien hand - moves independent of volitional control
Neglect to affected body part
Imbalance and loss of ambulatkon over time
Response to L dopa usually poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Pathology of corticobasal syndrome

A

Accumulation of tau in the brain, some overlap with Alzheimer’s pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Functionable tremor characterized as

A

Entrainable: When doing repetitive task with contralateral limn then tremor adopts frequency of the repetitive voluntary movements of that limb
Distractible: Can decrease while performing different tasks or during the intervention
Suggestible: Commencing examination exacerbates the tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Medications causing, triggering or unmasking tremor

A

valproate
Topiramate
Beta agonists (inhalers)
Lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Essential tremor prevalence

A

affects 4% of people age 40 and increasing with age
Often mild, generally progressive but can be debilitating
Autosomal family nistory common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Clinical features of essential tremor

A

bilateral action tremor (kinetic and postural components)
MUST FIRST develop in upper limns but can evolve to include head, jaw or vocal cords
Can be exquisitely responsive to alcohol
Only in one axis - which can be seen if you ask the patient to draw a spiral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Treating essential tremor

A

often respond well to propranolol.
Refractory severe cases maybe neuromodulation through DBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Young patient with tremor and prominent neuropsychiatric symptoms?

A

consider Wilson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Holmes tremor

A

Usually due to lesions in upper brainstem or thalamic structures.
Large amplitude unilateral and multimodal (resting and action) tremor, worsening remarkably with action.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Hemi body chroea

A

consider structural causes, eg severe hyperglycemic states, vascular leskoms and space occupying lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Generalized chorea with subacute onset

A

in children: Sydenham’s chorea post strep infections
In adults: SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Dystonia

A

abnormal cocontractkon of antagonistic muscles leading to abnormal postures or twisting and repetitive movements.
Tend to be activated by tasks at least initially
Can happen due to drug reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Components required for normal gait

A

Locomotor system (musculoskeletal system and motor ouput)
Sensory function, partic proprioception
Sensorimotor integration and cognition
Cardiopulmonary function
Attention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Inputs important for gait (afferents)

A

Proprioception via large peripheral nerve fibres traveling via dorsal columns in spinal cord
Vestibular system (linear and angular head movemrnts)
Visual system
Only two out of three are required, hence why removing vision (Rombergs) = loss of sensory function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

The gait cycle

A

Consists of a stance phase = double and single leg support alternate
Followed by a swing phase = occurs on single leg support, for forward propulsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Approach to investigating falls

A

was the fall associated with an abrupt loss of postural tone?
-with loss of consciousness (syncope, seizure, basilar occlusive disease)
-without loss of consciousness (drop attacks)
Does the patient have a history of unsteadiness?
-abnormality in structures involved in gait
-is there weakness, is this UMN or LMN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Patterns of gait difficulty in proximal LMN weakness (eg myopathies)

A

wide based, waddling gait, struggle to climb stairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Patterns of gait difficulty in distal LMN weakness (eg length dependent peripheral neuropathies)

A

Foot drop with steppage gait pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Patterns of gait difficultie in UMN weakness (spasticity)

A

short steps, struggle to lift feet off ground with circumduction of the affected limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Lesions in cerebellar hemispheres pattern

A

limb incoordination on the ipsilateral side of the lesion = hemispheric cerebellar syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

lesions in the medial cerebellum (vermis) pattern

A

Axial instability (body sway, head tremor)
Vestibular manifestations (dizziness, vertigo, nystagmus, double vision) if the flocculonodular lobe is affected
Nb. Limbs mat be unaffected, so absence of limn dysmetria/dysdiadokinesia does not rule out cerebellar disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Signals that ataxia (dyscoordination) is dud to a cerebellar lesion

A

Oculomotor abnormalities (saccadic dysmetria, vertical nystagmus, pure torsional or pure horizontal nystagmus)
Dysarthria (speech irregular in eate and amplitude, slurred, slow and segmented
Body sway (truncal instability) or head tremor
Limb incoordination (dysmetria, dysdiadokinesia, intention tremor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Ataxia due to sensory dysfunction in proprioception

A

Patients complain of balance difficult in dark environments, eg at night or when closing eyes in shower
Unsteady and ‘stomping’ gait eith heavy heel strikes can be seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

ataxia due to sensory dysfunction in vestibular system

A

Acute unilateral vestibular dysfunction can lead to pronounced vertigo, nystagmus and vomiting
Chronic bilateral vestibular failure can present with subtle disequilibrium and oscillopsia (objects appear to jump or vibrate with head movements )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Differentials for acute onset cerebellar ataxia

A

Stroke of posterior circulation
Younger patients can be post viral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Differentials for subacute onset (days to weeks) cerebellar ataxia

A

Areflexia - consider Miller Fisher syndrome
Signs of raised ICP - consider space occupying lesion
History of autoimmunity - there are a number of immune disorders causing cerebellar syndrome
History of cancer - paraneoplastic cerebellar degeneration Dan be first manifestation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Differentials for chronic cerebellar syndromes

A

Degenerative and inheritable conditions
After structural, toxic and nutritional causes have been excluded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Acquired causes disrupting PNS causing sensory ataxia

A

peripheral neuropathy
- length dependent (diabetes, paraproteinemia)
- non-length dependent (infectious, paraneoplastic)
Ganglionopathy (immune mediated (Sjogren’s), infectious (HIV))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Acquired causes inCNS causing sensory ataxia

A

Myelopathy (spinal cord lesions any cause eg inflammatory, infections, autoimmune, toxic)
-B12 or copper deficiency -> subacute combined degeneration cord syndrome with selective involvement of dorsal columns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Features of B12 myeloneuropathy

A

Sensory ataxia
Encephalopathy
Optic atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Ix in patients with cerebellar ataxia

A

MRI
consider LP in acute and subacute with no structural lesions, especially if possibility of immune mediated
Consider genetic test if chronic and positive FHx, or features suggestive of multisystem atrophy,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Ix for patients with sensory ataxia

A

MRI spine if suspect myelopathy
B12, copper, HIV and syphilis test in all patients
Neurophysiology if neuropathy suspected
- if NCS shows peripheral demyelinating neuropathy consider LP (immune mediated paraprotein, anyloid causesD
- axinal neuropahty then search for systemic condition eg diabetes, metabolic, nutritional deficiency
If vestibular dysfunction suspected consider
- vestib head impulse test
Audiometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Management of patients with ataxia

A

avoid precipitants like excess alcohol
Physio
OT
SALT
patient/carer educaiton/counselling

109
Q

Red flags in patient with neck/lower back pain

A

Age >50
History of signif trauma or recent manipulation (chiropractor)
Intractable pain at night or fest
Constitutional symptoms
History of cancer or suspect cancer
History of immunosuppression
History of foreign travel
History of osteoporosis
Progressive neurological symptoms

110
Q

Symptoms and signs of conus medullaris

A

Pain not common or severe, bilateral and symmetric in perineum and thighs
Sensory deficit saddle distribution bilaterally
Motor loss symmetric no marked, sometimes fasciculations
Ankle jerks lost
Early and marked bowel and bladder dysfunction

111
Q

symptoms and signs cauda equina

A

Spontaneous pain common and severe, mat be unilateral and asymmetric, in perk rum, thighs, legs, back, bladder, sacfal nerve distribution
Sensory deficit in saddle distribution but may be unilateral
Asymmetric motor loss, atrophy may occur, usually no fasciculations
Ankle and oafellar jerks loss
Bowel and bladder dysfunction relatively late

112
Q

Causes pointing to underlying mechanical cause of neck or back pain

A

Dull, midline pain
Lack of radiation in a dermatomal pattern, or no radiation

113
Q

Headache history

A

Types of headache
Position
Quality (throbbing? Severity?)
Timing
Radiation
Associated symptoms (nausea, photo/phonophobia, aura, cranial autonomic features)
Better (meds? Lying flat.)
Worse (cough? Activity? Orthostatic?)
Triggsrz

114
Q

Extra headache history qs if old

A

for GCA
Amaurosis fugax
Diplopia
Fever
Chills
Night sweats
Scalp tenderness
Jaw claudication
Tongue claudication
PMR
Chronic cough

115
Q

Red flags for headache

A

Head or neck injury
New onset/new type
New level of pain/abrupt onset
Headache during pregnancy
Age >50
Focal neurological signs or symptoms
Systemic illness
Secondary risk factors (cancer, immunocompromise, recent travel)

116
Q

Differentials for thunderclap headache

A

Subarachnoid hemorrhage
Intracerebral haemorrhage
Cerebral venous sinus thrombosis
Pituitary apoplexy
Carotid/vertebral artery dissection
CSF leaks
Spontaneous retrocoival haemaromas
Colloid cyst of third ventricle
Hypertensive encephalopathy

117
Q

Primary headaches

A

Migraine
Tension
Cluster

118
Q

Secondary headachws

A

Idiopathic intracranial hypertension
Giant cell arteritis
Medication overuse headache

119
Q

Diagnosis criteria for migraine

A

At least 5 attacks
Attacks last 4-72 hours
Two of:
-severe intensity
-unilateral
-throbbing
-activity worsens headache
One of:
-nausea and or vomiting
-photo/phonophobia
Not attributed to anything else

120
Q

Migraine aura

A

May be focal neurology, usually preceding:
-visual
-dysphagia
-somatosensory
-motor
-other
Develops over minutes and complete duration 15-20 mins

121
Q

Migraine treatment

A

Identify and eliminate triggers
Abortice treatment: Simple analgesics, 5-HT1 agonists (triptans, ergotamine), anto emetics, opiates
Preventative treatmenr: (basically if bad and recurrent)

122
Q

Tension type headache

A

mild to moderate intensity
No migrainous features
No cranial autonomic features
No secondary causes
Not exacerbated by daily activities
Treat
Aborticz: NSAIDs, acetaminophen
Prophylaxis: TCAs. Topiramate, valproic acid, gabapentin

123
Q

cCluster headache diagnosis

A

At least 5 attacks
Severe or unilateral orbital, supraorbital and/pr temporal pain lasting 15-180 mins if untreated
Usually sign things like lacrimation, nasal confesfion, owdema, sweating, ptosis etc
Really frequent, dg one every other day to 8 per day
No other cause

124
Q

Trigeminal neuralgia

A

Painful, unilateral shock pain im V2, V3 and a bit V1
Rapid onset/offset and lasting seconds
No sensory deficits or constant neuropathic pain
Triggered by wind, talking, chewing, touching
MRI w gadolinium required to exclude tumour, demyelination or stroke as cause

125
Q

Trigeminal neuralgia treatment

A

Carbemazepine is drug of choice
Surgery eg microvascular decompression or destruction trigeminal ganglion

126
Q

Idiopathic intracranial hypertension symptoms

A

symptoms of raised ICP (headache, oulsatile tinnitus, horizontal diplopia)
Symptoms of papilloedema (loss of perpipj vision, blurring, transient visual onscurations)

127
Q

Medication overuse headache diagnosis

A

headache occurring on at least 15 days per month in a patient with a pre-existing headache disorder
Regular overuse for >3 months of one or more drugs that can be taken for acute and or symptomatic treatment of headache
Not better accounted for by another diagnosis

128
Q

Risk factors for idiopathic intracranial hypertension

A

Female sex
Obesity
Reproductive age
Menstrual irregularity
Medications (cimetidine, corticosteroids, retinoic acid, minocycline, nitrofurantoin, trimethoprim and sulfamethoxazole)
Chronic renal insufficiency
SLE

129
Q

Clinical examination for idiopathic intracranial hypertension

A

Visual function testing w fundoscopy, visual field testing, visual acuity and colour testing
Ocular motility testing
Neurological examination

130
Q

Differential diagnoses for IIH

A

Dural venous sinus thrombosis
Intracerebral jazz lesion
Hydrocephalus
Meningeal infiltrative and inflammatory disease

131
Q

Treatment for IIH

A

Medical: Lifestyle modification and weight loss, medications (acetazolamide, topiramate)
Surgical
Optic nerve sheath fenestration
CSF shunt for refractory cases

132
Q

Examining cranial nerves in a comatose patient

A

ii: Ophthalmoscopic exam
Blink to threat
Ii and iii: Pupillary responses
Iii, iv, ci. Viii: Spontaneous extraocular movements, nystagmus, dysconjugate gaze, oculocephalic maneuve, caloric testing
V, vii: Corneal reflex, facial asymmetry, grimace response
Ix, x: Gag reflex

133
Q

Examination of sensory and motor in a comatose patient

A

Spontaneous movements
Withdrawal from painful stimulus

134
Q

Reflexes exam in comatose patient

A

Deep tendon reflexes
Plantar reflexes
Posturing reflexes
Special reflex in case of suspected spinal cord lesions

135
Q

GCS components

A

Eye opening: Spontaneous (4), to speech (3), to pain (2), no response (1)
Verbal response:
Oriented (5), sentences (4), words (3), sounds (2), no response (1)
Motor response: Obeys commands (6), localizes to pain (5), flexion withdrawal to pain (4), abnormal flexion ro pain (3), extension to pain (2), no response (1)

136
Q

Risk factors for delirium

A

Age >70
Dementia or mild cognitive impairment
Vision impairment
Hearing impairment
Functional limitation
Alcohol abuse
Malnourishment
Dehydration

137
Q

Iatrogenic precipitants for delirium

A

Use of restraints
Urinary catheter
Recent surgery
Sleep deprivation
Untreated pain
Drugs

138
Q

Red flags for delirium

A

Focal signs
Alcohol/malnourishment
History of epilepsy
Features suggestive of seizures
Prolonged over days kto weeks
Fever of unknown origin
Young patient

139
Q

Weekly alcohol limit in units

A

14 units

140
Q

Units for binge for Men and women

A

8 units for man and 6 for women

141
Q

Harmful drinking units per week

A

> 50 units/week for men, >35 units/weeks for women

142
Q

Alcohol bloods

A

AST:ALT ratio increased
Incr GGT and ALP
Macrocytic anaemia
Reduced platelets
Carbohydrate deficient transferrin

143
Q

Motivational interviewing in brief

A

Feedback - personal risk/interviewing
Responsibility - you need to make change
Advise to cut down
Menu - options to change behaviour and targets (drink free days, drink diary, cut 10% per week, identify risks, other activities, information about sefvices)
Empathic - listen and avoid confrontation
Self-efficacy- encourage and promote self belief

144
Q

When does lateral tentorial herniation happen

A

from unilateral expanding mass

145
Q

What causes subfalcine midline shift

A

early occurrence in unilateral space occupying lesion. Seldom any clinical effect

146
Q

What causes central tentorial herniation

A

midline lesion or diffuse swelling of cerebral hemispheres causes vertical displacement of the midbrain and diencephalon

147
Q

What causes tonsillar herniation

A

Subtentoiral expanding mass causes herniation of cerebellar tonsils through the foramen magnum

148
Q

Risks for subdural haemorrhage

A

Elderly
Alcoholics
Alzheimer’s
At risk for falls
Susceptibility to haemorrhage eg chronic liver disease

149
Q

Differentials for thunderclap haemorrhage

A

SAH
Meningitis
Intraparenchymal haemorrhage
Hypertensive encephalopathy
Arterial dissection
CSF leak

150
Q

Indications and contraindications for LP

A

Indict: Investigate for infection, 12h after SAH for xanthochromia
Contra:coagulopathy, mass lesion

151
Q

Roles specific to the left hemisphere

A

analytical and logical thinking
Language (except emotional prosody
Expression of emotion
Writing and speech if right handed

152
Q

Roles specific to the right hemisohere

A

spatial abilities
Comprehension of complicated patterns and drawings
Perceiving emotion

153
Q

Functions of the frontal lobe

A

higher order processing, decision making
Motor cortex (precentrral gyrus)
Broca’s area (in dominant hemisphere) expressive for speech
Supplementary motor area
Social graces/inhibition

154
Q

Functions of the parietal lobe

A

post central gyrus = sensory cortex
Supramarginal and anterior gyri of dominant hemisphere = Wernicke’s area (comprehension)
Non dominant = integratin of visuospatial awareness
Visual pathways pass through deeply
Posterior parietal cortex for planning movements

155
Q

Lesion of parietal lobe on left causes

A

impaired:
Two point discrimination, stereognosis, graphaesthesia, localisation of touch, position sense
Disorders of language
Gerstmann Syndrome: Finger agnosia, acalculia, right left disorientation, agraphia

156
Q

Lesions of parietal lobe on right causes

A

impaired:
Two point discrimination, stereognosis, graphaesthesia, localisation of touch, position sense
Disturbances in integration of personal and extrapersonal space
Hemispatial neglect
Constructional apraxia
Dressing apraxia

157
Q

Expressive speech

A

broca’s area

158
Q

Fluency of speech

A

Wernicke’s area

159
Q

What does the insular lobe do

A

part of the paralimbic group
Connects limbic cortex with neocortex
Receives visceral, taste and pain sensory information

160
Q

Role of the thalamus

A

powerful hub of integration
Eg w ascending reticular activating systems, basal ganglia, limbic system, somatosensory, auditory, visual, vestibular input and thalamocortical and corticothalamic projections’ so thalamic issues lead to broad spectrum of neurologic issues

161
Q

Clues for NMJ disorders

A

(eg Myaesthenia gravis and lambert Eaton myasthenic syndrome)
Generalized FATIGUABLE weakness
Unexplained ptosis, bulbar problems

162
Q

CN I issues - think…

A

Cold, parkinsons

163
Q

CN III, IV, V(1&2), VI think

A

Cavernous sinus

164
Q

CN V, VII, VIII think…

A

cerebellopontine angle - acoustic neuroma?

165
Q

CN VI think

A

this is a false localizing sign. Be careful

166
Q

CN IX, X, XI, XII thnk…

A

Base of skull

167
Q

Eye movements which nerve

A

LR6 SO4. Everything else 3
Lateral recurs abducts eye
Superior oblique depressed adducted eye

168
Q

CN III palys

A

down and out, and ptosis

169
Q

Horner’s syndrome

A

thjnk hidden pathology: Pancoast’s tumour, Central line into subclavian, damage to internal carotid (dissection after heading a football really hard)
= sympathetic chain lesion between brain and eye
-> ptosis, meiosis, anhydrosis

170
Q

Is it vasovagal syncopy?

A

prolonged upright position
Sweating prior to loss of consciousness
Pre syncopal symptoms
Pallor
Nausea

171
Q

Cardiac syncope

A

bewAre, less warning and quite abrupt
>10% risk of death per year
History of IHD?
Investigate w ECG as possibly long QT, HOCM

172
Q

More likely epileptic seuizure

A

stertorous breathing
Postictal confusion
Relatively short duration
Urinary incontinence and tongue bite can occur in either

173
Q

More likely non epileptic attack

A

long duration
Asynchronous movements
Pelvic thrusting
Side to side head/body movements
Closed eyes
Ictal crying
Memory recall

174
Q

Patient descriptions of non epileptic atracks

A

Metaphors of space/place patients go through
Resistance to focusing on individual seizure episodes, and only provide detailed description with prompting
Focusing on impact on their lives

175
Q

Patient description of epileptic seizures

A

depicting seizure as agent/force or event/situation
Volunteered detailed first person accounts of seizures

176
Q

Status epilepticus

A

any seizure longer than five mins
May have convulsive break but then resume without regaining consciousness
Excitotoxic danger so urgently end with high dose benzos
Identify cause
After benzos give usual medication
Once thirty mins have elapsed get ITU invovlved for midazolam/propofol infusion

177
Q

Prognosis of epilepsy

A

50-60% controllable with one anti epileptic drug
Intractable in 10-20%, temporal lobe surgery?

178
Q

Acute central bladder issues

A

flaccid, acontractile bladder
Reflex control of sphincter-> urinary retention, bladder distention, overflow incontinence

179
Q

Chronic central bladder issues

A

hyperreflexic spastic bladder. Urinary frequency and urge incontinence due to detrusor-sphincter dysnergia

180
Q

Most common type of brain tumour

A

Mets are most common
Partic: Lung, breast, bowel, , melanoma and kidney

181
Q

Most common primary brain tumour in adults

A

glioblastoma multiforme

182
Q

Imaging glioblastoma

A

Solid tumours with central necrosis and rim which enhances with contrast.
Disruption of blood brain barrier so assoc w vasogenic oedema

183
Q

Treatment of glioblastoma

A

surgical with post op chemo and or radio
Dex often for oedema
Prognosis is about a year

184
Q

Second most common primary brain tumour in adults

A

meningioma

185
Q

Features of meningioma

A

typically benign extrinsic tumours of CNS
Arise from arachnoid xap cells and typically located next to dura
Partic AR falx cerebei, superior sagittal sinus, convexity or skull base
Cause symptoms by compression rather than invasion

186
Q

Investigations and treatments for meningioma

A

ix with CT AND Mei
Treatment may be observation, radiotherapy or surgical resection

187
Q

Features of vestibular schwannoma

A

benign tumour arising from eighth cranial nerve
Often at cerebellopontine angle
Presents with hearing loss, facial nerve palsy and tinnitus
Assoc w neurofibromatosis type 2

188
Q

Most common primary brain tumour in children

A

pilocytic astrocytoma

189
Q

Feat of medulloblastoma

A

aggressive paediatric brain tumour
Arises within infratentorial compartment and spreads theohfh cns
Treated with surgical resection and chemo

190
Q

Pituitary adenoma fearures

A

benign tumours of pituitary gland
Micro = less than 1cm, macro = more
If secretory will present with consequences of hormone excess
If non secretory may be solely bitempral hemianopia due to crossing nasal fibres

191
Q

Investigation and treatment of pituitary adenomas

A

pituitary blood profile and Mei
Can be hormonal treatment or transphenoidal resection

192
Q

Craniopharyngoma features

A

most common paediateic supratentoorial tumour
Solid/cystic tumour derived from remnants of Rathke’s pouch,
Mt present with hormonal disturbance, symptoms of hydroceph or bitemporal hemianopia

193
Q

What is vestibular neuritis

A

neuropathy of vestibular system probably caused by reactivation of latent HSV1 in vestibular ganglion.
Always preceded by prior upper respiratory tract infection

194
Q

History vestibular neuritis

A

Sudden, spontaneous, severe ongoing vertigo
Not triggered by movement but may be exacerbated by it
Frequent nausea and vomiting
Hearing loss and tinnitus in labyrinthitis

195
Q

Symptoms to ask about which indicate more serious than vestibular neuritis or labyrinthitis

A

Otorrhoea with middle ear disease or head trauma
Otalgia = herpes zoster otichs
Neck pain/stiffness = meningitis or vertebral artery dissection
Cardiovascular risk factors increased likelihood of being stroke or TIA
Family nistory of migraine or Meniere’s make these more likely
Drugs eg aminoglycosides, amlodipine, amdtodepressants and antiepileptics can all cause vertigo

196
Q

Examination vestibular neuritis

A

Gait = tend to fall towards affected side when standing or walking
Weber’s test: Tuning fork on head, quieter In affected ear
Head impulse test: Get patient to fix their gaze on your nose then turn their head rapidly side to side. If intact zVOR then should be able to keep gaze on nose, if neuritis then will have catch up reflexive saccade
Horizontal nystagmus
HINTS exam

197
Q

HINTS examination

A

Head impulse test, nystagmus type and skew

198
Q

Vestibular neuritis management

A

resolves over days to weeks without treatment
If ant concerns like sudden onset unilateral hearing loss need to admit for possible acute ischaemia or labyrinth or brainstem
Otherwise reassure, and they can lie still with eyes closed during acute attack, prochlorperazine or antihistamines can help w vertigo nausea and vomiting

199
Q

What is meniere’s disease

A

disorder of inner ear caused by change in fluid volume in the labyrinth, generally with multifactorial, inexact cause. Most commonly middle aged and qhite rare.

200
Q

Symptoms of meniere’s disease

A

Vertigo, tinnofis and fluctuating hearing loss with a sensation of aural pressure.
Fluctuating and episodic nature is important, attacks are minutes to hours (2-3), and inclusters of 6-11 per year. Initially at least unilateral.

201
Q

Examination in Meniere’s diseae

A

there are no signs, but should examine cardiovascular, neuro and ENT systems to look for other causes of similar symptoms.

202
Q

Driving and vertigo

A

any vertigo = must notify DVLA , and case then considered individually depending on whether ant warning, severity and whether controlled.

203
Q

Treatment of Meniere’s disease

A

Acute atracks: vertigo and nausea with prochlorperazine or other anti emetic, mat need to be IM if vomiting, and may need fluid rehydration
Prophylasis: Lifestyle avoid salt, caffeine, chocolate, alcohol, tobacco and fatigue. Consider betahistine?
Can be really debilitating

204
Q

What is BPPV

A

most common cause of vertigo due to inner ear dysfunction. Otoliths detach and then circulate loosely in the semicicrcular canals so generating a sensation of ongoing movement
Affects approx 3% of people typically presenting in women age about 50

205
Q

History with BPPV

A

episodes of vertigo provoked by head movements eg rolling over in bed, lying down, sitting up, turning head in horizontal plane
Comes on suddenly (typically 5 secs after provocative movement) and lasts 20-30s and rapidly resolving if head kept still.
Nausea common
Symptoms typically worse in morning
No hearing loss, tinnitus, mastoid pain, headache or photophobia
May present as a fall

206
Q

Red flags with vertigo

A

unilateral hearing loss or tinnitus
New inset headache
Focal neurological signs
Cerebellar signs eg gait ataxia

207
Q

Dix hallpike manoeuvre

A

Ask patient to keep eyes open and look straight ahead. Sit on couch with head turned 45 degrees to one side
Then lay person down rapidly, supporting head and neck, until head is extended 20-30° over end of couch with chin up and test ear down
Observe eyes for 30 secs for nystagmus and note what it’s like
Provoking vertigo and upbeating nystagmus = zBPPV normallt 5-20 sec after manoeuvre

208
Q

Management of BPPV

A

advise symptoms ususallt self limiting over several weeks but may recur
Offer Epley’s manoeuvre
Advise no driving when dizzy ir if driving might provoke an attack

209
Q

Epley’s manoeuvre

A

Sit patient upright with head turned 45° to affected side
Place hands on either side of head and lie down with head 30° over edge of bed, wait 30 sec ti 1 min
Rotate head 90° to opposite side with patient’s face upwards
Then roll patient on to side whilst holding head in position then rotate head to face ground
Sit patient up sideways while maintaining head rotation (still facing geound)
Rotate heae to central position

210
Q

Midline cerebellar lesions symptoms

A

severe gait and truncal ataxia
If extending, fourth cranial nerve leskons, severe ipsilateral arm tremor, marked nystagmus, vertigo and vomiti g

211
Q

Cerebellar hemisphere lesions symptoms

A

ipsilateral limb ataxia (intention tremor, past pointing, mild hypotonia)
Limb rebound
Tend to be more subtle nystagmus

212
Q

Acute onset ataxia didferentials and presentation

A

cerebellar haemorrhage or infarction
Occipital headache, vertigo, vomiting, altered consciousness

213
Q

Subacute ataxia differentia’s

A

viral infection: Children age 2-10 wieth pyrexia, limb and gait ataxia and dysarthria appearing over hours to days and lasting up to 6 months
post infectious encephalomyelitis
Other options: Hydrocephalus, posterior fossa tumours, absecesses

214
Q

Differentials for episodic ataxiaa

A

may appear bizarre and seem a bit functional
episodic alone can develop in teenage years, lasting from minutes to hours anf usually triggered by something (eg stress, exercise, caffeine or alcohol)
Drugs
MS
Transient vertebrobzsilar ischaemic attacks
Foramen magnum compression

215
Q

Chronic progressive ataxias didferentials

A

commonly caused by chronic alcohol abuse associated with malnutrition, may improve with thiamine and poss other vitamins
Also drugs eg phenytoin
Solvent abuse
Heavy metals
Structural lesions
Paraneoplastic cerebellar degeneration sssociated with carcinomas of the lung or ovaries
CJD

216
Q

Examining for cerebellar signs

A

DANIISH: Dysdiadokinesia, ataxia, nystagmus, intention tremor, slurred staccato speech, hypotonia

217
Q

Causes if cerebellar dysfunction in infantsz

A

cerebral palsy
Intrauterine infection
Pontocerebellar hypoplasia
Joubert’s syndrome
Trisomies
Pyruvate dehydrogenase deficiency

218
Q

Friedrich’s ataxia

A

most common type of hereditary ataxia, affecting about 1/50000
Symptoms usually develop before age 25, and then worsen over time
Symptoms: Ataxia causing falls, dysarthria, increasing weakness in legs, dysphagia, vision and hearing loss, diabetes, hypertrophic cardiomyopathy, peripheral neuropathy

219
Q

Ataxia telangiectasia

A

rare hereditary ataxia
Symptoms begin in early childhood
Most need wheelchair by age 10
Increasing dysarthria and dysphagia
Telangiectasia in corner of eyes and on cheeks
Immunodeficient
Incr risk cancer partic ALL
Usual life expectancy 19-25

220
Q

Spinocerebellar ataxias

A

Group of hereditary ataxias that don’t begin until adulthood
Variable symptoms, but including ataxia, dysarthria, dysphagia, muscle stiffness and cramps, peripheral neuropathy , memory loss,slow eye mivenets, urinary urge or incontinence

221
Q

Weber’s test

A

512Hz tuning fork placed in middle of forehead
Normal: Sound is heard equallt in both ears
Sensorineural hearing loss: Sounds heard louder on side of intact ear
Conductive hearing loss: Sound is heard louder on side of the affected ear
To differentiate between these, perform Rinne’s test

222
Q

Rinne’s test

A

Place vibrating 512Hz tuning fork on mastoid process = test bone conduction
Confirm patient can hear, then ask then when can Bo longer hear it
Then move tuning fork in front of external auditory meatus to test for air conduction
They should then be able to hear sound again as air conduction is normally better than bone
If conductive hearing loss, bone conduction mat be better than air.

223
Q

Other tests for hearing loss

A

Pure tone audio entry (measures decibel and pitch hearing)
Typanometry is measure of stiffness of eardrum and evaluates middle ear functoon

224
Q

Qhat is sinusitis

A

inflammation of membranous lining of one or more sinuses, generally accompanied by inflammation of the nasal mucosa, but can be acute, recurring or chronic

225
Q

Acute sinusistis

A

bacterial or viral infection of sinuses lasting fewer than four weeks and then completely resolving
Rends to be viral, and then secondary bacterial infection with strep pneumo, h influenzae, and morazella
Common
Present with non resolving cold >1 week with pain in affected sinus (partic fullness feeling worse on bending forward), possibly phrexia, discharge from nose and loss of smell.
Mostly reassure and give paracetamol/ibuprofen, a week of intranasal decongestant, nasal irrigation and warm face packs

226
Q

History for vertigo

A

first attack
Duration
Precipitating factors
Otologic symptoms
Medications
Age

227
Q

Acoustic neuromas

A

2-30/ million
Slowly progressive
Up to 50% don’t grow ar all
Present with; unilateral sensorineural hearing loss, unilateral tinnitus, Imbalance, unilateral facial nerve weakness, unilateral trigeminal paraesthesia

228
Q

More likely to be syncope than seizure?

A

prolonged upright position
Sweating prior to LOC
pre syncopal symptoms
pallor
Nausea
Can be postural, reflex or cardiac (which is more dangerous and rends to have less of a warning prodrome)

229
Q

Seizures and the DVLA

A

Always have to have 6 months off driving after first seizure (even if likely cardiovascular)
And if epilepsy must have 12 monrhs seseizure free

230
Q

Investigations for epilepsy

A

CT/MRI
EEG - is this generalized epioepsy? Is there a specific focus? Is it non convulsive status?
ECG

231
Q

Common side effecrs of carbemazepine

A

rash
Hyponatraemia
Cardiac conduction issues
Increased ADH
Pancytopaenia
Hepatotoxicity
Dizziness, unsteadiness, cramps

232
Q

Side effects of phenytoin

A

gingival hypertrophy
Rash
Peripheral neuropathy
Pancytopaenia
Hepatotoxicity

233
Q

Side effects of lamotrigine

A

rash - needs slow titration
Tremor

234
Q

Side effects of levetiracetam

A

mood disturbance - low mood, aggressive behaviour

235
Q

EEG in epilepsy

A

Demonstrates abnormal cortical excitability
Electrodes placed on scalp reflect asummation fexexcitatory inhibitory postsynaptic neurons at most superficial layer of cortex, and need relatively large areas to be activated at the same time in order to pick up activity
Hence specific but not sensitivity

236
Q

Features of temporal lobe seizures

A

slow head turn at onset (towards seizure focus?)
Automatisms (fidgeting, picking)
nose wiping
Ictal spitting, vomiting, coughing

237
Q

Frontal lobe seizures

A

Jacksonian seizures: March of limb jerking spread
Speech arrest or dysphagia suggest dominant bemisphere involvement

238
Q

First line treatments forparkinsons

A

If motor symptoms affecting patients QoL: Levodopa
If motor symptoms not affecting patients QoL: Dopamine agonist ( eg bromocroptine, ropinirole, cabergoline) levodopa, or MAO-B inhibitor (eg selegiline)

239
Q

Relative benefits of levodopa vs dopamine agonists vs MAO B inhibitors

A

levodopa more improvement in motor symptoms and ADLs
But levodopa also more motor complicatkons
dopamine agonists: More adverse events (excessive sleepiness, hallucinations, impulse control disorders)

240
Q

Impulse control disorders in Parkinsons

A

can occur with any dopaminergic therapy but more common with:
Dopamine agonist therapy
History of previous impulsive behaviours
History of alcohol consumption and/or smoking

241
Q

Levodopa info

A

nearly always combined with decarboxylase inhibitor eg carbidopa to precent peripheral metabolism of dopamine outside brain
Common adverse effecrs: Dry mouth, anorexia, palpitations, postural hypotension, psychosis
Plus effects from difficult achieving steady dose: Wearing off, and then to on off phenomenon, with dyskinesia at peak dose
Do not stop acutely asrisk of acute dystonias

242
Q

Dopamine receptor agonists info

A

Parkinson’s meds
eg bromocriptine, ropinirole, cabergoline, apomorphine
Bromocriptine nd cabergoline are ergot derived and have been assic w pulmonary, retroperitoneal and cardiac fibrosis. Do echo, ESR, creatinine and CXR before trearment
Risk of impulse control disorders and excessive somnolence
More likely than levodopa to cause hallucinations in older patients

243
Q

MAO-B inhibitors

A

Parkinson’s nedicarjons
Eg selegiline
Inhibits breakdown of dopamine secreted by dopaminergic neurons

244
Q

Amantadine

A

Parkinson’s medication
Mechanism not fully understood, probably increases dopamine release and inhibits its uptake at dopaminergic synapses
Side effecrs: Ataxia, alurred speech, confusion, dizziness, livedo retivularis

245
Q

COMT- inhibitors

A

Parkinson’s medication
Eg entacapone, tolcapone
COMT is enzyme involved in breakdown of dopamine so can be used as adjunct to levodopa therapy, in established PD

246
Q

Peripheral neuropathy causing predominantly motor loss

A

guillain Barre syndrome
Chronic inflammatory demyelinating polyneuropathy
Porphyria
Lead poisoning
Hereditary sensorimotor neuropathies eg Charcot Marie Tooth
Diphtheria

247
Q

Peripheral neuropathy causing predominantly sensory loss

A

diabetes
Uraemia
Leprosy
Alcoholism
Vitamins B12 deficiency (subacute combined degeneration of cord-> loss of joint position and vibration first from dorsal column
Amyloidosis

248
Q

MRI investigations for MS

A

demonstrations of lesions disseminated in time and space
Contrast MRI -> high signal T2 lesions
CSF-> oligonclonal bands (not in serum), increased intrathecal synthesis of IgG

249
Q

Common peroneal nerve lesoom

A

foot drop
Weakness of dorsiflexion
Weakness of foot eversion
Weakness of extensor hallucis longus
Sensory loss over dorsum of foot and lower lateral part of leg
Wasting of anterior tibial and peroneal muscles

250
Q

Chronic myopathy (inherited) oresenfe and absence of symptoms

A

proximal weakness
Proximal atropjy
Ptosis present
rarelY displopia
frequent head drop
Normal to mildly elevated CK

251
Q

Subacute myopathy presence and absence of symptoms

A

proximal weakness
no atrophy
Rarely ptosis
No diplopia
Frequent head drop
very high CK

252
Q

AAnterior horn syndromes features

A

WEAKNESS: Pure LMN pattern, can affect any limb. Mat see wasting
Additional fearures: Fasciculations, bulbar symptoms (dysphagia, dysarthria) +/- tongue wasting
May have respiratory faikure

253
Q

Possible causes of anterior horn syndromes

A

Spinal muscular atrophy
Early stages amylotrophic lareral sclerosis
Acute flaccid myelitis - eg viral: Polio, west nile virus

254
Q

Multifocal motor neuropathy features

A

onset can be indistinguishable from anterior horn syndromes
Distribution of weakness: typically distal predominant with late wasting. Preference for upper limbs and very distal (fingers). Not typically bulbar symptoms

255
Q

What is multifocal motor neuropatht

A

Rare disorder of autoimmune attack on multiple motor nerve, ttypically starting with asasymmetrical weakness in the patient’s hands
Antibody to GM1
Few sensory symptoms
Chronically progressive without remission
Very similar to CIDP but onset asasymmetric and not remitting

256
Q

Treatment of multifocal motor neuropathy

A

IVIg or plasma exchange, ongoing every 2-5 weeks

257
Q

Guillain Barre syndrome chcharacterized

A

Rapid onset ascending weakness, numbness and oaralysis of limbs, respiratory muscles and face
lost reflexes
50% after microbial infectiom

258
Q

Neuromuscular junction diseases features

A

distribution of weakness: typIcaloy proximal, fluctuates and often worse towards the end of the day
ffatiguable weakness
Frequent ptosis
extraocular muscle iinvolvement > complex ophthalmoplegia
Bulbar involvement > dysarthria and dysphagia
Not typically muscke atrophy

259
Q

Differentials for neuromuscular junction weakness

A

myasthenia gravis = immune mediated by antibody against ACh receptor or rarely anti-MUSK
Lambert Eaton myasthenic syndrome = antibodies to Ca channels. Frequently paraneoplastic
Botulism = neuroparalytic toxin rare in West simetines home canned foods
Congenital/inherited forms are rare

260
Q

Cervical myeloradiculopathy

A

ususually following cervical/spinal trauma
Course is static and progression halts after some time
LMN findings in cervical/upper thoracic region plus UMN sign s in lower limbs
MRI: Myelopathy plus multiple nerve root involvement

261
Q

Diagnosis of GBS

A

lumbar puncture for elevated protein AND normal WCC
EMG

262
Q

Treatment of GBS

A

unpredictable, so unless very mild, need to be hospitalised to monitor respiration
Plasma exchange and IV Ig can be helpful to shorten the course
Mat well need lots of rehab, OT, social work and psychiatry input
Possible long term recurrence of fatugue and exhaustion

263
Q

CIDP what is

A

Progressive autoimmine polyneuropathy with distal and proximal weakness and sesensory deficit developing over at least 8 weeks
Underlying cause not known but thought to be deranged immune response causing perioheralperipheral in damage
Can be pure motor or sensory oresentations

264
Q

DifDifference between guillain barre and CIDP

A

guillain barre: Onset less than 4 weeks
Often clinical history of infection prior to onset of symptoms
More commonly involves cranial nerves and respiratory failure than CIDP

265
Q

Treatment for CIDP

A

corticosteroids 60mg OD pred six weeks
plasma exchange and IV Ig for relief from symotoms
Approx 15% patients fail to respond to treatment

266
Q

Becker muscular dystrophy

A

x linked recessive dystrophinopathy. Less severe version of Duchenne
Develops after age of 10, and intellectual impairment much less common than in duchenne

267
Q

What is charcot Marie tooth

A

most common hereditary peripheral neuropathy
results in predominantly motor loss
No cure and management focused on physical and occupational therapy

268
Q

Clinical fearures of charcot Marie tooth

A

history of frequently sprained ankles
foot drop
High arched feet (pes cavus)
Hammer toes
Distal muscle weakness
Distal muscle atrophy
Hyporeflexia
Stork leg deformity

Year 5 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions