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Core clinical problems > 14. abnormal/unsteady gait > Flashcards

14. abnormal/unsteady gait Flashcards

1
Q

name some abnormal gaits

A

equinas
high stepping
antalgic
trendelenberg
parkinsonian
ataxic
hemoplegic
diplegic

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2
Q

presentation equinas

A

“equine dressage”
This is where one foot is tip-toeing - heel not touching the ground

This is because the ankle is unable to dorsiflex

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3
Q

presentation high stepping gait

A

This is where the knees are brought up high so as to be able to place the heel down
The ankle has weakness of dorsiflexion so compensated through to avoid tripping

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4
Q

presentation antalgic gait

A

“the quick step”
This is where one leg spends little time in the stance phase due to pain

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5
Q

presentation trendelenberg gait

A

Caused by weak lower limb abductors
Pelvis fails to rise on lifted leg causing pt to compensate with upper body leaning over
(look at shoulder position

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6
Q

presentation parkinsonian gait

A

Slow initiation
Short step length
Reduced arm swing
“Shuffling gait”
Rigidity and bradykinesia

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7
Q

presentation ataxic gait

A

Broad base, staggering

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8
Q

presentation hemiplegic gait

A

Spastic flexion of UL and extension of LL
Due to extension of the lower limb, the leg is elongated meaning patients have to swing their leg round to prevent it dragging

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9
Q

presentation diplegic gait

A

flexion of UL and extension of LL on both sides leading to legs being swung around to avoid dragging

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10
Q

causes equinas gait

A

This is because the ankle is unable to dorsiflex

Cerebral palsy
Tight achilles eg in talipes
Limb length discrepancy
Autism spectrum disorder

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11
Q

causes of drop foot/high stepping gait

A

Direct injury to dorsiflexors
Common peroneal nerve injury
L5 radiculopathy
Peripheral neuropathy - motor loss predominant

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12
Q

causes antalgic gait

A

any cuase of lower limb pain

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13
Q

causes trendelenberg gait

A

L5 radiculopathy (weakness of hip abduction)
Painful hip pathology eg trochanteric bursitis
Femur neck fracture
Hip dislocation
Proximal muscle weakness but more so if unilateral

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14
Q

causes parkinsonian gait

A

parkinsons disease

drug induced parkinsonism

parkinsons plus syndromes (MSA and supranuclear pasly)

Normal pressure hydrocephalus

Lewy body dementia

Parkinsons dementia

wilsons disease

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15
Q

causes ataxic gait

A
  • cerebellar
  • sensory due to loss of proprioception (dorsal column sign)
  • vestibular
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16
Q

causes hemiplegic gait

A

Cerebral palsy hemiplegic

CNS lesion
- Stroke
- Space-occupying lesion
- Trauma
- MS

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17
Q

causes diplegic gait

A

Spinal cord lesion
MND
Bilateral brain lesion

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18
Q

how to ddx the most common causes of footdrop

A

most common = common peroneal nerve palsy

L5 radiculopathy (weakness of hip abduction is suggetsive)

other causes: motor loss peripheral neuropathy

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19
Q

Presentaion guillian barre syndrome

A

symptoms:
- progressive symmetrical ascending weakness
- can have leg pain/back pain
- mild distal paraesthesia

signs:
- reflexes reduced or absent
- reduced sensation in a glove and stocking distribution

there may be a history of gastroenteritis

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20
Q

what is guilian barre

A

Guillain-Barre syndrome describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni).

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21
Q

what additional features of guillian barre should you check for? worrying ones?

A

respiratory muscle weakness
signs of DVT/PE

cranial nerve involvement
diplopia
bilateral facial nerve palsy
oropharyngeal weakness is common
autonomic involvement
urinary retention
diarrhoea

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22
Q

invetsigations ?guilian abrre

A

lumbar puncture
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%

nerve conduction studies may be performed
- decreased motor nerve conduction velocity (due to demyelination)
- prolonged distal motor latency
- increased F wave latency

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23
Q

LP findings guillian barre

A

rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%

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24
Q

nerve conduction findings guillian barre

A

decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency

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25
Q

management of guillian barre

A

IV immunoglobulins or plasma exchange

VTE prophylaxis (pulmonary embolism is a leading cause of death)

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26
Q

leading cause of death in guillian barre

A

pulmonary embolism

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27
Q

presentation of miller fischer carient of guillian barre

A

progressive proximal weakness and a triad of ophthalmoplegia, areflexia and ataxia

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28
Q

what is the most common hereditary peripheral neuropathy

A

Charcot-Marie-Tooth Disease

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29
Q

features of charcot-marie tooth

A

There may be a history of frequently sprained ankles
Foot drop
High-arched feet (pes cavus)
Hammer toes
Distal muscle weakness (especially ankle dorsiflexion)
Distal muscle atrophy (inverted champagne bottle legs)
Hyporeflexia
Stork leg deformity
Reduced tone
Peripheral sensory loss

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30
Q

why does charcot amrie tooth affect peripheries first

A

Because longer nerves are affected first, symptoms usually begin in the feet and lower legs and then can affect the fingers, hands, and arms.

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31
Q

gait charcot marie tooth

A

may have foot drop/high stepping gait

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32
Q

type 1 vs type 2 charcot amrie tooth? what does this mean for invetsigation interpretation

A

type 1 demyelinating therefore reduced conduction velocity in nerve conduction studies

type 2 axonal

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33
Q

pathophysiology charcot marie tooth

A

CMT is caused by mutations in genes that support or produce proteins involved in the structure and function of either the peripheral nerve axon or the myelin sheath.

Because longer nerves are affected first, symptoms usually begin in the feet and lower legs and then can affect the fingers, hands, and arms.

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34
Q

inheritance charcot marie tooth

A

autosomal dominant

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35
Q

investigation charcot marie tooth

A

nerve conduction studies (slow in t1)

genetic testing

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36
Q

presentation lead poisoning

A

Abdominal pain, peripheral neuropathy motor, blue lines on gum margin

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37
Q

parkinsonian syndrome presentation

A

Tremor (resting)
Rigidity
Bradykinesia
Postural instability (imbalance)

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38
Q

tremor parkinsons

A

Resting tremor: improves with voluntary movement, pill-rolling tremor, worse when stressed or tired

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39
Q

triad of parkinsons

A

bradykinesia, tremor, rigidity

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40
Q

how to differneitate aprkinsons and drug induced parkinsonism

A

parkinsons disease= slow onset, asymmetrical

drug induced = fast onset, symmetrical

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41
Q

pathophysiology parkinsons disease

A

Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra

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42
Q

presentation parkinsons disease

A

Triad of: bradykinesia, tremor, rigidity
Classically asymmetrical symptoms
Resting tremor: improves with voluntary movement, pill-rolling tremor, worse when stressed or tired
Rigidity : lead pipe, cogwheel due to superimposed tremor
Difficulty with fine movements
Mask-like facies
Flexed posture
Micrographia
Drooling of saliva
Psychiatric: depression (affects 40%), dementia, psychosis, sleep disturbances
Impaired olfaction
REM sleep behaviour disorder
Fatigue
Autonomic dysfunction: postural hypotension

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43
Q

o/e parkinsons

A

general inspection: resting tremor (pill rolling), mask like facies, flexed posture

function = Difficulty with fine movements, micrographia

gait: shuffling, bradykinesia

tone = rigidity, lead pipe rigidity, cog-wheel rigidity due to superimposed tremor

power = normal
sensation = normal
reflexes = normal

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44
Q

management parkinsons disease

A

For first-line treatment:

if the motor symptoms are affecting the patient’s quality of life: levodopa

if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

45
Q

what are the 3 types of drugs used parkinsons

A

levodopa

dopamine agonists

MAO-B inhibitors

46
Q

what is on/off phenomenen parkinsons disease

A

On/off phenomenon in Parkinson’s disease happens when the common treatment levodopa wears off and motor symptoms return, before it’s time for your next dose.

47
Q

name a non-ergot derived dopamine agonist

A

ropinorole

48
Q

name some ergot derived dopamine agonists. what is the problem with these?

A

(bromocriptine, pergolide, cabergoline) - require monitoring due to fibrosis SE

49
Q

disadvantages of dopamine agonists in parkinsons

A

more risk of hallucinations, compulsive behaviour, postural hypotension, daytime sleepiness, specific ergot side effects of fibrosis

50
Q

disadvantages of levodopa

A

More motor complications such as dystonia, chorea and athetosis

51
Q

examples of MAOB inhibitors? how do they work

A

Selegiline
Rasagiline

Prevent breakdown of dopamine and can be used alongside levodopa

52
Q

MoA levodopa

A

Levodopa crosses the blood brain barrier where it is converted to dopamine by decarboxylation in the presynaptic terminals of dopaminergic neurons.

53
Q

what drugs can cause drug induced parkinsonism

A

Antipsychotics or antiemetic metoclopramide

54
Q

antiemetic for parkinsons

A

domperidone as it doesn’t cross BBB therefore doesn’t cause EPSE

55
Q

features multiple system atrophy (PP)

A

Parkinsonism
Autonomic disturbance : erectile dysfunction often early feature, postural hypotension, atonic bladder
Cerebellar signs eg ataxia

56
Q

types of multiple system atrophy

A

MSA-P - Predominant Parkinsonian features

MSA-C - Predominant Cerebellar features

57
Q

fetaures supranucelar palsy (PP)

A

Postural instability and falls
Stiff, broad-based gait
Impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficulty reading or descending stairs)
Parkinsonism: bradykinesia prominent
Cognitive impairment, primarily frontal lobe dysfunction

58
Q

presentation normal pressure hydrocephalus

A

“Wet, wobbly and weird”
Urinary incontinence
Gait abnormality (shuffling and freezing)
Dementia and bradyphrenia (slowness of thought)

59
Q

pathophysiology normal pressure hydrocephalus

A

Reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.

60
Q

normal pressure hydrocephalus iamging results

A

ventriculomegaly in the absence of, or out of proportion, with sulcal enlargement

(sulcal enlargement and ventricular enlargement is normal in elderly (atrophy) in NPH, the ventricles are larger out of proportion

61
Q

management normal pressure hydrocephalus

A

ventriculoperitoneal shunting (VP shunt)

around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhage

62
Q

features lewy body dementia

A

progressive cognitive impairment

parkinsonism

visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

63
Q

how does the cognitive impairment in lewy body differ from alzhimers

A

in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
cognition may be fluctuating, in contrast to other forms of dementia

64
Q

invetsigation lewy bodyd ementia

A

SPECT/DaTSCAN

65
Q

management of lewy body dementia

A

Both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.

66
Q

difference between LBD and PDD

A

Lewy body. cognitive decline –> parkinsons

Parkinson’s disease dementia. parkinson’s –> cognitive decline

67
Q

age presentation of wilsons, differences in presentation

A

Age 10-25 years
Children: liver disease (acute liver failure or chronic picture)
Young adults: neurological disease

68
Q

features wilsons disease

A

Liver:
hepatitis, cirrhosis
Neurological:
basal ganglia degeneration → parksinonsom
Speech, behavioural and psychiatric problems
Asterixis, chorea, dementia
Kayser-Fleischer rings:
Green-brown rings in the periphery of iris due to copper accumulation in descemet membrane
Renal tubular acidosis
Haemolysis
Blue nails

69
Q

nails wilsons disease

A

blue nails

70
Q

inheritance wilsons

A

Autosomal recessive disorder

71
Q

genetics wilsons disease

A

Defect in ATP7B gene located on chromosome 13

Autosomal recessive disorder

72
Q

wilsons disease copper studies interpretation

A

Low ceruloplasmin and low total serum copper as this is proxy for ceruloplasmin
Increased free (non-ceruloplasmin-bound) serum copper is increased
Increased urinary excretion of copper

73
Q

management wilsons disease

A

Penicillamine (chelates copper)

74
Q

presentation ataxia

A

“without coordination”

75
Q

examiantion if there is features of ataxia

A

?cerebellar
do cerebellar exam DANISH

?sensory
rombergs test
neuro exam ?spinal signs ?peripheral neuropathy

?vetsibualr
rombergs test
associated vertigo?
assess hearing

76
Q

cerebellar signs

A

Dysdiadochokinesia
Ataxia - definition = “without coordination”
Nystagmus
Intention tremor
Slurred speech
Hypotonia

77
Q

what is an important cerebellar cause of ataxia that you need to rule out in new onset ataxia

A

stroke

Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)

Ipsilateral: facial pain and temperature loss, Contralateral: limb/torso pain and temperature loss, Ataxia, nystagmus

PICA
Pain Ipsilateral
Contralateral ataxia

MEDullary = MEDical attention for burns

78
Q

causes of sensory loss peripheral neuropathy

A

A – Alcohol
B – B12 deficiency
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. amiodarone, metronidazole, cisplatin, phenytoin, isoniazid, nitrofurantoin)
E – Every vasculitis

79
Q

presentation diabetic peripheral neuropathy

A

Distal Symmetrical Sensory Neuropathy
Most common
Caused by loss of large sensory fibres.
Sensory loss in a glove and stocking distribution.
Often affecting touch, vibration and proprioception.

Small-fibre Predominant Neuropathy
Caused by loss of small sensory fibres.
Presents with deficits in pain and temperature sensation in a glove and stocking distribution along with episodes of burning pain.

80
Q

diabetic with erratic blood glucose control, bloating and vomiting?

A

Gastroparesis
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)

81
Q

management of painful diabetic peripherla neuropathy

A

Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain:
1. amitriptyline, duloxetine, gabapentin or pregabalin
2. if the first-line drug treatment does not work try one of the other 3 drugs
+ tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems

82
Q

diabetic with postural hypotension, urinary retention?

A

Autonomic Neuropathy

Presents with postural hypotension, gastroparesis, constipation, urinary retention, arrhythmias and erectile dysfunction.

83
Q

what spinal cord disorders may lead to ataxic gait

A

anything that damages the dorsal columns and therefore impairs proprioception

  • myelopathy
  • subacute combined degeneration
  • friedrich’s ataxia
  • tabes dorsalis
84
Q

presentation subacute combined degenration of the spinal cord

A

bilateral dorsal column signs - seonsory disturbance (paresthesia, pain etc.), loss of fine touch, proprioception, vibration,

may have bilateral corticospinal tract signs (affects posterior cord) - UMN signs eg hypertonia, hyperreflexia, weakness in pyramidal pattern

85
Q

prevention subacute combined degenration

A

Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord

86
Q

presentation friedrichs ataxia

A

teenager - same pattern as subacute combined degenertaion of spinal cord

bilateral dorsal column signs - loss of fine touch, proprioception, vibration

may have bilateral corticospinal tract signs (affects posterior cord) - UMN signs eg hypertonia, hyperreflexia, weakness in pyramidal pattern

spinocerbellar also does proprioception and is affected so ataxia may be quite prominent

cerebellar signs as also damages cerebllum DANISH

87
Q

inheritance and genetics friedrichs ataxia

A

autosomal recessive trinucleotide repeat disorder resulting in reduced level or function of the frataxin protein.

88
Q

presentation of tabes dorsalis

A

dorsal columns affected

Loss of proprioception and vibration sensation = ataxic gait, parasthesia,

triad of:
unsteady gait, lightening-type pains, and urinary incontinence/sexual dysfunction

Other symptoms that may occur include seizures, stroke, behavioral changes, headache, dizziness, and hearing impairment.

89
Q

if ataxia is vestibular, what other symptom is usually present?

A

Ataxia from the vestibular system is almost always associated with vertigo

and slow nystagmus with or without change of position. Affected patients also tend to veer to the ipsilateral side when they try to walk in a straight line. Hearing loss should be further evaluated to rule out inner ear issues.

90
Q

define cerebral palsy

A

a disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain.

91
Q

causes cerebral palsy

A

antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)
intrapartum (10%): birth asphyxia/trauma
postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma

92
Q

presentation cerebral palsy child

A

abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulties.

93
Q

assciated non-motor symptoms of cerebral palsy

A

learning difficulties (60%)
epilepsy (30%)
squints (30%)
hearing impairment (20%)

94
Q

most common type of cerebral palsy

A

spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons

95
Q

other than spastic cerebral palsy, what other types are there? pathophysiology

A

dyskinetic
caused by damage to the basal ganglia and the substantia nigra
athetoid movements and oro-motor problems
ataxic
caused by damage to the cerebellum with typical cerebellar signs
mixed

96
Q

management of cerebral palsy

A

MDT approach

treatments for spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery and selective dorsal rhizotomy

anticonvulsants, analgesia as required

97
Q

clues which point to a diagnosis of motor neurone disease

A

fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common

Other features
doesn’t affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature

98
Q

pathophysiology motor neurone disease

A

There are several theories and explanations. There is degeneration of the motor neurones (UMN and LMNs). Part of this degeneration is particularly seen in the ventral/anterior portion of the spinal cord.

eg in ALS

Motor cortex neuronal cell damage causes upper motor lesion signs, and anterior horn cell damage causes lower motor lesion signs, which explains the mixed signs seen in ALS. Sole damage to either of these areas would only cause one type of motor neurone lesion sign. Multiple lesions of the brain are commonly seen in multiple sclerosis.

99
Q

name UMN lesion signs

A

Weakness ‘Pyramidal’ pattern i.e. weakness of upper limb extensors, lower limb flexors
Hyperreflexia of deep tendon reflexes- as no UMN regulating that reflex
Absent superficial reflex - babinski positive
Hypertonia + or - clonus (Spasticity occurs in pyramidal tract lesions) such as clonus and clasp-knife rigidity
Pronator drift

100
Q

name LMN signs

A

Muscle atrophy
Flaccid paralysis
No plantar response
Absent tendon reflexes
Fasciculations (single muscle fibres of uninjured LMN stimulated)
?glove and stocking
Focal pattern of weakness i.e. only muscles innervated by damaged neurones are affected

101
Q

what is pronator drift indicative of?

A

upper limb weakness due to an upper motor neurone lesion

contralateral side

102
Q

how to make a diagnosis of motor neurone disease? ddx?

A

The diagnosis of motor neuron disease is clinical, but nerve conduction studies will show normal motor conduction and can help exclude neuropathy. Electromyography shows a reduced number of action potentials with increased amplitude.
MRI is usually performed to exclude the differential diagnosis of cervical cord compression and myelopathy

103
Q

ALS presentation

A

Amyotrophic lateral sclerosis (50% of patients most common) -

typically LMN signs in arms and UMN signs in legs

104
Q

primary lateral sclerosis presentation

A

UMN signs only

105
Q

progressive muscualr atrophy presentation

A

LMN signs only
affects distal muscles before proximal
carries best prognosis

106
Q

progressive bulbar palsy presentation

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

107
Q

subtypes of motor neurone disease?

A

amyotrophic lateral sclerosis - LMN in arms, UMN in legs

priamry lateral sclerosis - UMN only (l before m so upper)

priamry muscualr atrophy - LMN only

Progressive bulbar palsy - palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei

108
Q

management of MND

A

Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months

Resp care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months

109
Q

what type of drugs are contraindicated in LBD

A

neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent

Core clinical problems (94 decks)

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