Limb weakness Flashcards
What things might get confused with limb weakness?
- Limb ataxia
- Limb numbness (reduced sensation)
- Limb pain - too painful to move
What are the time courses for the onset of limb weakness and suggest how this could reflect the potential pathologies?
- Sudden onset (seconds to minutes) - suggests traumatic (e.g. displaced vertebral fractures) or vascular insults (e.g. stroke, TIA)
- Subacute onset (hours to days) - progressive demyelination (Guilla-Barre or MS) or a slowly expanding haematoma
- Chronic onset (weeks to months) - slow growing tumour or motor neurone disease
Outline the neuro-anatomical pathway from the motor cortex all the way down to the muscle cells
- M1 (primary motor cortex)
- Corona radiata
- Internal capsule
- Pons (via cerebral peduncles)
- Medulla - point of decussation for 90% of fibres
- Down the spinal cord in the corticospinal tract
- Nerve roots and plexus
- Neuromuscular junction
- Muscle
DDx (see notes)
What things are important to elicit from a neurological history in someone with limb weakness, and why?
- Time / onset?
- Visual / speech disturbance?
- Indicates central disturbance rather than spinal cord or periphal nerves
- Headache?
- Unusual in vascular causes - stroke or TIA
- Sudden-onset, terrible headache - subarachnoid haemorrhage
- Unilateral headache preceding limb weakness - hemiplegic migraine
- Gradual-onset headache preceding limb weakness - intracranial mass such as slowly expanding subdural haemorrhage
- Seizure or loss of consciousness?
- Not typical of stroke
- Todd’s paresis (post-seizure) stroke mimic
- Hypoglycaemia
- Neck or back pain?
- Suspect spinal pathology such as…
- Spontaneous disc prolapse
- Traumatic injury to the spine
- Discitis
- Spinal abscess
- OR Guillan-Barre
- Head Trauma?
- Subdural haemorrhages - including slowly expanding subdural haemorrhages in elderly patients
- Risk factors for stroke?
- Previous stroke / TIA
- AF
- Atherosclerotic risk factors
- Migraine with aura
- SLE
Outline the different UMN and LMN signs
UMN
- ↑ Tone
- ↑ Reflexes
- ↑ Plantars (Babinski’s reflex)
- Clonus (sometimes)
HOWEVER, important to note that the acute phase of UMN pathologies cause hypotonia and hyporeflexia, as in LMN pathologies, and only then do they progress to hypertonia and hyperreflexia
LMN
- ↓ Tone
- ↓ Reflexes
- Fasciculations (sometimes)
- Wasting
1) The presence of language defects suggests pathology in which general region?
2) What are the 2 types of language defects - describe these and identify which specific area of the brain is affected?
1)
- Cortex of the dominant hemisphere (usually left, even in left handed people)
2)
- Receptive (Wernicke’s) dysphagia - the patient speaks fluently (although with jumbled words / phrases) but cannot comprehend language
- Lesion in Wernicke’s area (in the temporal lobe) of the dominant hemisphere
- Expressive (Broca’s) dysphagia - the patient can comprehend language and follow instructions, but cannot find words or speak fluently
- Lesion in Broca’s area (in the frontal lobe) of the dominant hemisphere
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Describe what occurs in attention defects and where these localise pathologies to
- Patient appears to be ignoring half of their sensory world (e.g. responding only to cues on one side of the bed)
- Parietal cortex lesion
Outline the neuroanatomy for vision (also draw this out)
- Retina
- Nerve fibres from nasal and temporal aspects of each eye
- These converge at the optic nerve
- Most fibres decussate at the optic chiasm, however some remain ipsilateral
- Then down via optic tracts
- To the LGN (Lateral Geniculate Nucleus)
- Optic radiations
- Occipital lobe
Where is the lesion in a patient with complete blindness in one eye in terms of neural visual field defects?
- Optic nerve
Where is the lesion in a patient with homonymous hemianopia in terms of neural visual field defects?
- In the ipsilateral optic tract OR
- The contralateral occipital lobe
Where is the lesion in a patient with bitemporal hemianopia?
- Optic chiasm
If there is eye deviation in the context of limb weakness
1) Towards the weak limb
2) Away from the weak limb
What does this suggest in terms of localisation of the lesion?
1)
- Cortical lesion
2)
- Brain-stem lesion
How can sensory signs help diagnosis in LMN and UMN lesions?
LMN
- Nerve root / peripheral nerve lesion - sensory signs present
- Neuromuscular / muscular lesion - sensory signs absent
UMN
- Damage to specific spinal cord tracts
- Spinothalamic (pain and temperature paraesthesia)
- Dorsal column (light touch, vibration, position sense or proprioception paraesthesia)
- Therefore, for example anterior spinal artery infarct spares the dorsal column so these sensory modalities are spared
What does the following suggest, facial nerve palsy and
1) Forehead involvement and bilateral blinking problems?
2) Forehead sparing and no bilateral blinking problems?
1)
- LMN lesion - final common pathway to the frontalis and orbicularis muscle is destroyed
- OR bilateral UMN lesion?
2)
- Unilateral UMN lesion
1) Based on the motor homunculus, what would stroke in the anterior cerebral artery and middle cerebral artery cause?
2) Also what else would infarct of the middle cerebral artery (MCA) cause based on it supplying another neuroanatomical structure - and what is this structure?
1)
- Anterior cerebral artery supplies the medial M1 and therefore based on the motor homunculus might affect the lower limb
- Middle cerebral artery - lateral M1 and therefore, based on teh motor homunculus, might affect the thorax all the way up to the face, tongue and pharynx as you go more lateral
2)
- Supplies the right posterior parietal cortex, where damage can cause contralateral hemineglect
Why are carotid bruits of interest in a limb weakness picture?
- Carotid bruits could be due to aortic stenosis OR carotid artery atheromas
- Emboli point to vascular causes such as TIA or stroke
