14. abnormal/unsteady gait Flashcards
name some abnormal gaits
equinas
high stepping
antalgic
trendelenberg
parkinsonian
ataxic
hemoplegic
diplegic
presentation equinas
“equine dressage”
This is where one foot is tip-toeing - heel not touching the ground
This is because the ankle is unable to dorsiflex
presentation high stepping gait
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
presentation antalgic gait
“the quick step”
This is where one leg spends little time in the stance phase due to pain
presentation trendelenberg gait
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
presentation parkinsonian gait
Slow initiation
Short step length
Reduced arm swing
“Shuffling gait”
Rigidity and bradykinesia
presentation ataxic gait
Broad base, staggering
presentation hemiplegic gait
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
presentation diplegic gait
flexion of UL and extension of LL on both sides leading to legs being swung around to avoid dragging
causes equinas gait
This is because the ankle is unable to dorsiflex
Cerebral palsy
Tight achilles eg in talipes
Limb length discrepancy
Autism spectrum disorder
causes of drop foot/high stepping gait
Direct injury to dorsiflexors
Common peroneal nerve injury
L5 radiculopathy
Peripheral neuropathy - motor loss predominant
causes antalgic gait
any cuase of lower limb pain
causes trendelenberg gait
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
causes parkinsonian gait
parkinsons disease
drug induced parkinsonism
parkinsons plus syndromes (MSA and supranuclear pasly)
Normal pressure hydrocephalus
Lewy body dementia
Parkinsons dementia
wilsons disease
causes ataxic gait
- cerebellar
- sensory due to loss of proprioception (dorsal column sign)
- vestibular
causes hemiplegic gait
Cerebral palsy hemiplegic
CNS lesion
- Stroke
- Space-occupying lesion
- Trauma
- MS
causes diplegic gait
Spinal cord lesion
MND
Bilateral brain lesion
how to ddx the most common causes of footdrop
most common = common peroneal nerve palsy
L5 radiculopathy (weakness of hip abduction is suggetsive)
other causes: motor loss peripheral neuropathy
Presentaion guillian barre syndrome
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
what is guilian barre
Guillain-Barre syndrome describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni).
what additional features of guillian barre should you check for? worrying ones?
respiratory muscle weakness
signs of DVT/PE
cranial nerve involvement
diplopia
bilateral facial nerve palsy
oropharyngeal weakness is common
autonomic involvement
urinary retention
diarrhoea
invetsigations ?guilian abrre
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
LP findings guillian barre
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
nerve conduction findings guillian barre
decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency
management of guillian barre
IV immunoglobulins or plasma exchange
VTE prophylaxis (pulmonary embolism is a leading cause of death)
leading cause of death in guillian barre
pulmonary embolism
presentation of miller fischer carient of guillian barre
progressive proximal weakness and a triad of ophthalmoplegia, areflexia and ataxia
what is the most common hereditary peripheral neuropathy
Charcot-Marie-Tooth Disease
features of charcot-marie tooth
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
why does charcot amrie tooth affect peripheries first
Because longer nerves are affected first, symptoms usually begin in the feet and lower legs and then can affect the fingers, hands, and arms.
gait charcot marie tooth
may have foot drop/high stepping gait
type 1 vs type 2 charcot amrie tooth? what does this mean for invetsigation interpretation
type 1 demyelinating therefore reduced conduction velocity in nerve conduction studies
type 2 axonal
pathophysiology charcot marie tooth
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.
inheritance charcot marie tooth
autosomal dominant
investigation charcot marie tooth
nerve conduction studies (slow in t1)
genetic testing
presentation lead poisoning
Abdominal pain, peripheral neuropathy motor, blue lines on gum margin
parkinsonian syndrome presentation
Tremor (resting)
Rigidity
Bradykinesia
Postural instability (imbalance)
tremor parkinsons
Resting tremor: improves with voluntary movement, pill-rolling tremor, worse when stressed or tired
triad of parkinsons
bradykinesia, tremor, rigidity
how to differneitate aprkinsons and drug induced parkinsonism
parkinsons disease= slow onset, asymmetrical
drug induced = fast onset, symmetrical
pathophysiology parkinsons disease
Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra
presentation parkinsons disease
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
o/e parkinsons
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
management parkinsons disease
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
what are the 3 types of drugs used parkinsons
levodopa
dopamine agonists
MAO-B inhibitors
what is on/off phenomenen parkinsons disease
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.
name a non-ergot derived dopamine agonist
ropinorole
name some ergot derived dopamine agonists. what is the problem with these?
(bromocriptine, pergolide, cabergoline) - require monitoring due to fibrosis SE
disadvantages of dopamine agonists in parkinsons
more risk of hallucinations, compulsive behaviour, postural hypotension, daytime sleepiness, specific ergot side effects of fibrosis
disadvantages of levodopa
More motor complications such as dystonia, chorea and athetosis
examples of MAOB inhibitors? how do they work
Selegiline
Rasagiline
Prevent breakdown of dopamine and can be used alongside levodopa
MoA levodopa
Levodopa crosses the blood brain barrier where it is converted to dopamine by decarboxylation in the presynaptic terminals of dopaminergic neurons.
what drugs can cause drug induced parkinsonism
Antipsychotics or antiemetic metoclopramide
antiemetic for parkinsons
domperidone as it doesn’t cross BBB therefore doesn’t cause EPSE
features multiple system atrophy (PP)
Parkinsonism
Autonomic disturbance : erectile dysfunction often early feature, postural hypotension, atonic bladder
Cerebellar signs eg ataxia
types of multiple system atrophy
MSA-P - Predominant Parkinsonian features
MSA-C - Predominant Cerebellar features
fetaures supranucelar palsy (PP)
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
presentation normal pressure hydrocephalus
“Wet, wobbly and weird”
Urinary incontinence
Gait abnormality (shuffling and freezing)
Dementia and bradyphrenia (slowness of thought)
pathophysiology normal pressure hydrocephalus
Reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.
normal pressure hydrocephalus iamging results
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
management normal pressure hydrocephalus
ventriculoperitoneal shunting (VP shunt)
around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhage
features lewy body dementia
progressive cognitive impairment
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
how does the cognitive impairment in lewy body differ from alzhimers
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
invetsigation lewy bodyd ementia
SPECT/DaTSCAN
management of lewy body dementia
Both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.
difference between LBD and PDD
Lewy body. cognitive decline –> parkinsons
Parkinson’s disease dementia. parkinson’s –> cognitive decline
age presentation of wilsons, differences in presentation
Age 10-25 years
Children: liver disease (acute liver failure or chronic picture)
Young adults: neurological disease
features wilsons disease
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
nails wilsons disease
blue nails
inheritance wilsons
Autosomal recessive disorder
genetics wilsons disease
Defect in ATP7B gene located on chromosome 13
Autosomal recessive disorder
wilsons disease copper studies interpretation
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
management wilsons disease
Penicillamine (chelates copper)
presentation ataxia
“without coordination”
examiantion if there is features of ataxia
?cerebellar
do cerebellar exam DANISH
?sensory
rombergs test
neuro exam ?spinal signs ?peripheral neuropathy
?vetsibualr
rombergs test
associated vertigo?
assess hearing
cerebellar signs
Dysdiadochokinesia
Ataxia - definition = “without coordination”
Nystagmus
Intention tremor
Slurred speech
Hypotonia
what is an important cerebellar cause of ataxia that you need to rule out in new onset ataxia
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
causes of sensory loss peripheral neuropathy
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
presentation diabetic peripheral neuropathy
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.
diabetic with erratic blood glucose control, bloating and vomiting?
Gastroparesis
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)
management of painful diabetic peripherla neuropathy
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
diabetic with postural hypotension, urinary retention?
Autonomic Neuropathy
Presents with postural hypotension, gastroparesis, constipation, urinary retention, arrhythmias and erectile dysfunction.
what spinal cord disorders may lead to ataxic gait
anything that damages the dorsal columns and therefore impairs proprioception
- myelopathy
- subacute combined degeneration
- friedrich’s ataxia
- tabes dorsalis
presentation subacute combined degenration of the spinal cord
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
prevention subacute combined degenration
Always replace vitamin B12 before folate - giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord
presentation friedrichs ataxia
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
inheritance and genetics friedrichs ataxia
autosomal recessive trinucleotide repeat disorder resulting in reduced level or function of the frataxin protein.
presentation of tabes dorsalis
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.
if ataxia is vestibular, what other symptom is usually present?
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.
define cerebral palsy
a disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain.
causes cerebral palsy
antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)
intrapartum (10%): birth asphyxia/trauma
postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma
presentation cerebral palsy child
abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulties.
assciated non-motor symptoms of cerebral palsy
learning difficulties (60%)
epilepsy (30%)
squints (30%)
hearing impairment (20%)
most common type of cerebral palsy
spastic (70%)
subtypes include hemiplegia, diplegia or quadriplegia
increased tone resulting from damage to upper motor neurons
other than spastic cerebral palsy, what other types are there? pathophysiology
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
management of cerebral palsy
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
clues which point to a diagnosis of motor neurone disease
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
pathophysiology motor neurone disease
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.
name UMN lesion signs
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
name LMN signs
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
what is pronator drift indicative of?
upper limb weakness due to an upper motor neurone lesion
contralateral side
how to make a diagnosis of motor neurone disease? ddx?
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
ALS presentation
Amyotrophic lateral sclerosis (50% of patients most common) -
typically LMN signs in arms and UMN signs in legs
primary lateral sclerosis presentation
UMN signs only
progressive muscualr atrophy presentation
LMN signs only
affects distal muscles before proximal
carries best prognosis
progressive bulbar palsy presentation
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis
subtypes of motor neurone disease?
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
management of MND
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
what type of drugs are contraindicated in LBD
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
