Routine for examination of lower limbs:
Inspect (wasting, fasciculations, wheelchair/walking aid, catheter, pes cavus, limb shortening, inverted champagne bottle appearance)
Gait and Rhomberg’s test
Sensation (sensory level, joint position sense and vibration)
If time allows and you suspect flaccid paraparesis proceed as follows:
Back: sacral dimple, tuft of hair, scoliosis
Face: test CN VII, observe for ptosis, test eye movements, test fatiguability
Hands: wasting, coordination
Present to the examiner:
This patient has a flaccid paraparesis as evidenced by:
Reduced tone bilaterally
Wasting and weakness bilaterally
The patient was (un)able to walk. There was a wheelchair/walking aid by the bedside
There was (no) sensory loss
There were (no) cerebellar signs
With regards to aetiology:
There were (no) fasciculations to suggest motor neuron disease
There was (no) limb shortening to suggest polio
There was (no) sensory level to suggest cauda equina syndrome
There was (no) evidence of pes cavus and/or inverted champagne bottle appearance and/or scoliosis and/or hand muscle wasting to suggest charcot-marie tooth disease
There was (no) ptosis, opthalmoplegia, facial weakness to suggest guillain-barre syndrome or myasthenia gravis
There was (no) fatiguability to suggest myasthenia gravis
There were (no) cutaneous signs of spina bifida
To complete my examination I would like to:
Ask about bladder and bowel function
PR examination (if sensory level)
Assess speech and swallow and Forced vital capacity
Perform full neurological examination of upper limbs and cranial nerves (if not already done)
Causes of Flaccid Paraparesis:
*Think anterior horn cell—nerve root—plexus—peripheral nerve—NMJ—muscle*
- Anterior horn cell disease e.g. motor neuron disease (NB: mixed upper and lower motor neuron signs), poliomyelitis
- Cauda Equina Syndrome secondary to disc herniation/epidural abscess/mets/haematoma etc.
- Lumbosacral plexopathy secondary to trauma/tumour/abscess (usually unilateral)
- Motor neuropathies:
- Inflammatory: guillain-barre syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy, sarcoid, vasculitis, paraprotein, amyloidosis
- Infectious: HIV, diphtheria, lyme disease, HTLV-1, west nile virus, rabies, enteroviruses
- Toxins: lead, arsenic, thallium, mercury, shellfish, pufferfish poisoning
- Metabolic: diabetic amyotrophy, porphyria
- Drugs: ciclosporin, gold, penicillamine
- Congenital: charcot marie tooth disease (HSMN)
- Neuromuscular junction disorders:
- Myaesthenia gravis
- Lambert-Eaton myaesthenic syndrome
- Organophosphate poisoning
- Tick paralysis
- Snake venom
- Inflammatory: polymyositis/dermatomyositis. NB: can overlap with other connective tissue disease eg mixed connective tissue disease
- Other connective tissue disease eg. SLE, vasculitis, RA, systemic sclerosis.
- Cancer (paraneoplastic: carcinomatous neuromyopathy)
- Drugs (statins, steroids)
- Infections (bacterial infections, HIV, CMV, EBV, Hepatitis)
- Endocrine (thyroid, addisons, osteomalacia, cushings, acromegaly, diabetic amyotrophy)
- Toxins (alcohol)
- Metabolic (renal/liver failure, electrolyte disturbance e.g. periodic paralysis)
- Miscellaneous (inclusion body myositis, rhabdomyolysis, sarcoidosis, mitochondrial myopathy, muscular dystrophy)
- Spina Bifida (lumbosacral lesion)
Investigations according to most likely cause:
BP, L+S BP, ECG
Spirometry (FVC), ABG, CXR
EMG and Nerve conduction studies looking at velocity and amplitude
Bloods: peripheral neuropathy screen (see “Station 3 Peripheral Neuropathy”), CK, anti-AChR, anti-ganglioside antibodies
Neuro imaging (exclude cauda equine syndrome)
Lumbar puncture to examine CSF (raised protein in guillain-barre for example)
Hereditary Sensory Motor Neuropathy (Charcot Marie Tooth Disease):
Inherited peripheral neuropathy (motor>sensory)
Autosomal dominant mainly
CMT type 1. Chromosome 17. Mutation in PMP22 gene. Demyelination (reduced velocity on nerve conduction studies).
Causes distal wasting of legs (inverted champagne bottle appearance) and hands (clawed appearance) with weakness and mild sensory loss (can have sensory ataxia with positive Rhombergs) and areflexia. Bilateral foot drop with high-stepping gait. Bilateral pes cavus and toe clawing. Scoliosis. Occasionally palpable peripheral nerves.
Management: Multidisciplinary (physio, OT, geneticist, neurologist, orthopaedics, orthotics), analgesia, orthopaedic procedures
Guillain-Barre Syndrome (GBS):
An acute inflammatory demyelinating polyneuropathy
Onset over days- weeks. Following infection (often respiratory eg. M. pneumoniae/diarrhoeal illness eg. campylobacter)
Spinal pain, distal paraesthesiae, fatigue, ascending flaccid limb weakness, areflexia. Sensory deficits usually mild/patchy.
Cranial Nerves: ptosis, opthalmoplegia, facial nerve, bulbar weakness
Autonomic: tachycardia, labile BP, arrhythmias, bladder and bowels
Resp: SOB and fatigue.
NB: miller-fischer syndrome is a proximal variant of GBS causing ataxia, opthalmoplegia, areflexia (anti-GQ1b antibodies)
Can also get a sensory variant of GBS.
Investigations: albuminocytological dissociation in CSF (raised protein with normal WCC), reduced velocity and conduction block on NCS, antibodies to gangliosides (anti-GM1), vital capacity, ECG
Management: ITU if vital capacity <1.3L/bulbar dysfunction. May need tracheostomy, NGT. Give IVIG +/- methylprednisolone, or plasma exchange.
Becomes chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) if doesn’t cease by 6 weeks.
Cauda Equina Syndrome:
Compressed lumbosacral nerve roots below the level of the cord (disc herniation, trauma, tumour, abscess, inflammation, spinal stenosis for example)
Causing low back pain, sciatica, saddle anaesthesia, bladder and bowel and sexual dysfunction, flaccid paraparesis and areflexia.
Asymmetrical flaccid paraparesis with associated sensory loss (often L5, S1) and bladder/bowel involvement. Cutaneous signs of spina bifida include tufts of hair, dimples.
Neural Tube defect (incomplete closure of vertebral canal). Folic acid deficiency and sodium valproate use in pregnancy.
Flaccid monoparesis. Often associated limb shortening. No sensory loss. Differential = infantile hemiplegia
Polio is an enterovirus. Faecal-oral route of transmission. Predilection for anterior horn cells. Vaccine now exists.
Differential diagnosis of pes cavus (indicating long standing problem):
Charcot Marie Tooth disease
Written by Dr Sarah Kennedy
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