Limb Weakness History
Author – Dr Karthikeyan Sivaganesh Editor – Dr James Mackintosh
Last updated 05/05/24
Table of Contents
Introduction
Limb weakness can be categorised as functional, such as conversion syndrome, or pathological, due to muscle weakness, which can be primary, such as myositis, myopathy muscular dystrophy, or secondary, due to neuronal death, neuronal dysfunction and peripheral vascular disease.
Total muscle weakness, i.e. MRC rating of 0/5, is defined as paralysis and words end in “-plegia” e.g. hemiplegia, whereas partial muscle weakness is called paresis, which is much more common.
UMN vs LMN Signs
When considering a neurological cause of limb weakness, it is important to distinguish between an upper motor neuron (UMN) lesion or lower motor neuron (LMN) lesion.
UMN lesion | LMN lesion | |
Tone | Increased (spastic paresis) | Decreased (flaccid paresis) |
Weakness | Largest muscle group affected first i.e. upper limb extensors and lower limb flexors | Focal pattern i.e. only muscles innervated by the neuron are affected |
Reflexes | Increased | Decreased/absent |
Babinski (upgoing plantar) | Positive | Negative |
Other signs | Pronator drift, clonus (>5 beats is pathological) | Muscle wasting, fasciculations |
Typical Histories of Common OSCE conditions
UMN Condition
| Condition | Typical History |
|---|---|
Cerebral Stroke | Sudden onset hemiplegia/hemiparesis with
risk factors such as age >65 years, vasculopathy, thrombophilia, atrial fibrillation |
Multiple Sclerosis | Young woman, with history of autoimmune disease, internuclear ophthalmoplegia with UMN signs, asymmetrical sensory loss and cerebellar signs such as intentional tremor. |
Spinal Cord Lesion | Spastic paraplegia (unable to move lower parts of the body) below the lesion. Note, at the level of the lesion, there will be LMN signs. |
LMN Condition
| Condition | Typical History |
|---|---|
Peripheral Neuropathy | Typically symmetrical sensorimotor loss secondary to poorly controlled diabetes, alcohol misuse, vitamin B12 deficiency (e.g. pernicious anaemia), infections e.g. HIV, GBS |
Radiculopathy | History of slipped/herniated vertebral disc, osteoporosis, multiple pregnancies with sensorimotor deficits in a dermatomal pattern. |
Proximal Myopathy | History of endocrine disease such as Cushing’s syndrome, Addison’s disease or use of corticosteroids for rheumatological conditions such as polymyalgia rheumatica. |
Charcot-Marie-Tooth Disease | Positive family history with foot and hand deformities such as pes cavus (high arched foot) as they develop contractures (stiffened joints) |
Mononeuritis Multiplex | Asymmetrical sensorimotor loss (like multiple sclerosis) secondary to LMN damage such as diabetes, vasculitis, SLE |
Mixed UMN and LMN Condition
| Condition | Typical History |
|---|---|
Motor Neuron Disease | Elderly (>60 years) presenting with UMN and LMN signs only such as dysarthria, weakness, fasciculation, hypertonia |
Subacute Combined Degeneration of Spinal Cord | Features of pernicious anaemia or use of recreational drugs such as nitrous oxide causing vitamin B12 deficiency. Presents with deficits in the spinocerebellar tract (e.g. poorly coordinated movement), corticospinal tract (e.g. weakness) and dorsal columns (loss of proprioception, vibration with positive Romberg’s test). |
Friedreich’s Ataxia | Child (<15 years) with pes cavus, kyphoscoliosis, upgoing plantars, hyporeflexia and positive family history. |
Presenting Complaint
Site
Unilateral weakness e.g. stroke, plexus lesions such as Erb’s palsy
Bilateral weakness
- Autoimmune – myasthenia gravis, Lambert-Eaton syndrome, Guillain Barre syndrome, multiple sclerosis
- Cord compression – syringomyelia, degenerative cervical myelopathy
- Idiopathic – motor neuron disease
- Proximal predominance – polymyositis, Cushing’s disease, steroid-induced myopathy, statin-induced myopathy, muscular dystrophy, polymyalgia rheumatica
- Distal predominance – peripheral neuropathy such as diabetic neuropathy, mononeuritis multiplex or peripheral vascular disease
Dermatomal distribution e.g. nerve root compression causing radiculopathies
Onset
Early childhood/adolescence – muscular dystrophy, multiple sclerosis
Late adulthood – motor neuron disease (>60 years), stroke
Character
Shooting pain radiating down the leg – sciatica
Dull pain – spinal stenosis
Timing
Sudden onset:
- Trauma
- Ischaemic or haemorrhagic stroke
- Infection e.g. Guillain Barre syndrome
- Malignancy e.g. metastatic spinal cord cord compression
Gradual and progressive:
- Infection e.g. cerebral abscess
- Neurodegeneration e.g. MND, multiple sclerosis (MS)
- Malignancy e.g. growing tumour
Relapsing-remitting e.g. MS
Associated Symptoms
Back pain e.g. cauda equina syndrome, spinal stenosis, sciatica
Back pain and fever e.g. discitis, spinal abscess
Weakness with no sensory deficits e.g. MND
Precipitating Factors
Pain is worse walking downhill and improves bending forward → spinal stenosis
Viral/bacterial infection specifically Campylobacter → GBS
Difficult delivery (e.g. shoulder dystocia), swinging child by arms → Klumpke’s/Erb’s palsy
Red Flags
Bladder or bowel dysfunction e.g. cauda equina syndrome
Acute, focal neurological deficits e.g. stroke
Nocturnal headache, headache worse on lying down e.g. space-occupying lesion
Progressive weakness e.g. CNS tumour, MND, MS
Worsening back or thoracic pain e.g. spinal cord metastases
Fever, night sweats, rigors e.g. epidural abscess
Background
In any history you will ask about past medical history, medications, allergies, social history, and family history. In a history around fever in children, you can show how much you know about the various causes by explicitly asking about the following things:
Past Medical History
Diabetes → diabetic neuropathy
Malignancy → spinal cord or brain metastases
Thrombophilia → ischaemic stroke
Steroid use/statin use → proximal myopathy
Autoimmune disease e.g. type 1 diabetes → myasthenia gravis, multiple sclerosis
Family History
Charcot-Marie-Tooth disease
Friedreich’s ataxia
Social History
Recreational drug use e.g. nitrous oxide → subacute combined degeneration of spinal cord
IV drug use → discitis, epidural or brain abscess
Alcohol misuses → alcohol neuropathy, B12 deficiency
Significant history of smoking tobacco → Lambert-Eaton syndrome
Examination of Limb Weakness
Have a set of differentials prior to examining so you can rule in or out depending on the signs you elicit. Remember common is common! The aim of OSCE’s to assess your ability to identify common conditions and practice as a safe doctor e.g. not sending someone home if your suspect spinal cord compression.
Inspection
- Consider their age and gender and observe their gait and how they stand up from sitting.
- Look for fasciculations and muscle atrophy. The presence suggests a LMN lesion.
- For example, an elderly man with unilateral fixed flexion of the upper limb and fixed extension of the lower limb with circumduction is highly suggestive of stroke.
- If the person has difficulty standing up from a sitting position, it is suggestive of proximal muscle weakness.
Palpation
- Assess tone, power and reflexes for motor neuron function
- Consider the differential stated above depending on the signs elicited
- Assess sensory modalities e.g. pin-prick, crude touch, vibration and proprioception
- A sensorimotor deficit suggests multiple nerves are affected e.g. radiculopathies, peripheral neuropathies, mononeuritis multiplex, multiple sclerosis, etc
- Hamed Khan et al. OSCE’s for medical finals
- Davidson’s Principles and Practice of Medicine, 24th Edition