Approach to patient with neurologic disease Flashcards
Which clinical features of myopathy can be elicited by history?
What findings can be expected on examination of myopathy?
Myopathy causes proximal symmetric weakness without sensory loss
- Ask about: proximal leg weakness - Can patient get out of car, off the toilet, up from the chair w/o using hands?
- Ask about: proximal arm weakness - Can the patient lift or carry objects, such as grocery bags, garbage bags?
- Weakness should affect both arms and legs (often can be asymmetric, but weakness confined to one limb is unsual for myopathy)
- Normal sensation - can have pain/cramping but no sensation loss
Exam findings
- Proximal symmetrical muscle weakness without sensory loss
- No atrophy or fasciculations, muscle tone normal. Reflexes normal or mildly decreased.
Which clinical features of neuromuscular junction disease can be elicited by history?
What examination findings can be found on NMJ disease?
Fatiguability is hallmark. Strength will improve with rest, therefore it presents as a waxing and waning process rather than a progressive decline in function.
Exam
Fatiguable proximal symmetric weakness without sensory loss.
- Repetitive testing weakens muscle
- Extremely proximal weakness, involving face, eyes, jaw.
- Muscles normal in size, no atrophy or fasciculations, with normal tone and reflexes. There is NO sensory loss.
Which clinical features of peripheral neuropathies can be elicited by history?
What findings can be expected on examination?
Unlike myopathy and NMJ, weakness caused by peripheral neuropathies are often distal rather than proximal. Asymmetric and accompanied by atrophy and fasciculations.
- Distal leg weakness: trip, drag feet or wear out toes of shoes?
- Distal arm weakness: does patient frequently drop things or have trouble with grip?
- Asymmetric weakness: Glove and stocking symmetric, but most neuropathies are asymmetric.
- Denervation changes: Wasting or shrinkage of msucle, or quivering and twitching within muscle?
- Sensory changes: has patient felt numbness, tingling or parasthesia?
Exam
Distal, asymmetric weakness, with atropy and fasciculations, and sensory loss.
Muscle tone may be normal but often decreases, reflexes diminished.
Involvement of autonomic fibres is common. Look for smooth shiny skin, vasomotor changes, loss of hair or nails.
Which clinical features of radiculopathies (root diseases) can be elicited by history?
What can you find on examination?
Pain (sharp stabbing shooting) is the hallmark of root disease. Aside from this, they resemble peripheral neuropathy, with asymmetric weakness and evidence of denervation (LMN) and sensory loss. Weakness can be proximal or distal depending on root involved.
Exam
Asymmetric weakness in a myotomal distribution with LMN signs and sensory loss following a dermatomal distribution.
Which clinical features of spinal cord disease can be elicited by history?
What will you find on examination?
Usually cause triad of symptoms.
- Sensory level is the hallmark of spinal cord disease
- Distal, symmetric, and spastic weakness - UMN lesion affecting the corticospinal tract.
- Bowel and bladder problems
- Look for a sensory level, below which all sensory modalities are diminished
- Because most leg fibres lie laterally and easily compressed, spinal disease usually affects the legs more than the arms
- Level of symptoms detected may not correspond with anatomical site of injury
- Urinary retention or incontinence
- Lose superficial reflexes including anal wink
Important things to ask on history
- Distal leg weakness
- Distal arm weakness
- Symmetric process
- Sensory level
- Sphincter dysfunction
Which features of brain stem disease can be elicited by history?
What will you find on examination?
Cranial nerves characterise brainstem disease. Brain stem is like the spinal cord but embedded with cranial nerves.
Major long tracts run through - pyramidal, spinothalamic, dorsal column. Lesions in brain stem don’t produce horizontal motor or sensory level - but a vertical one; hemiparesis or hemianesthesia affecting one side of body.
What to look for on exam:
- Long tract signs - hemiparesis or hemisensory loss
- Cranial nerve signs - diplopia, dysarthria, dysphagia, dizziness, deafness, decreased strength or sensation over the face
- Crossed signs - brain stem lesions produced symptoms on one side of the face and opp side of the body
Which clinical features of cerebellar disease can be elicited by history?
What can you find on examination?
Incoordination, clumsiness, tremor - cerebellum responsible for smoothing out and refining movements.
- Clumsiness in legs: Ataxic, wide-based, staggering gait.
- Clumsiness in the arms: Difficulty with targeted movements - worse with voluntary, intentional movements
- Brain stem symptoms: Cerebellar inflow and outflow must pass through the brain stem and blood supply to the cerebellum arises from same vessels
How does pattern of motor and sensory deficits differentiate cortical from subcortical involvement?
Think about homunculus - lower extremeties reside between two hemispheres in the interhemispheric fissue, whereas neurons involving the trunk, arms and face are draped upside down over the superficial cortex.
Cortical lesions therefore affect the face, arm, and trunk but spare the legs. Incomplete hemiparesis.
Fibres to the leg descend and merge with the rest of the tract to form the pyramidal tract > internal capsule > cerebral peduncles > pyramids. Therefore small subcortical lesions can cause hemipareis - face, arm and leg.
Sensory homunculus is similar.
How does the type of sensory deficit differentiate cortical from subcortical lesions?
Most of the primary sensory modalities reach “consciousness” in the thalamus and do not require the cortex for their perception. A patient with severe cortical damange can still feel pain, touch, vibration, and position. A history of significant numbness or sensory loss, therefore, suggests subcortical lesion.
Cortical sensory loss is more refined and usually involves more complicate sensory processing such as two-point discrimination, accurate localisation of perceptions, stereognosis, and graphasthesia.
How do visual symptoms differentiate cortical from subcortical disease by history?
Visual pathways run subcortically for most of their length. Optic nerve > chiasm > optic tracts > lateral geniculate bodies > optic radiations > occipital cortex.
Cortical lesions that affect motor strip, sensory strip, or language areass are too superficial to affect visual fibres. If a lesion in the occiptal lobe - generally doesn’t have motor/sensory symptoms.
How can you differentiate cortical and subcortical disease on examination?
- Cortical dysfunction: aphasia, agraphia, acalculi, L-R disorientation, finger agnosia
- Motor: face and arm in cortical lesion, face, arm and leg in a subcortical lesion
- Sensory: deficit in primary sensory modalities in subcortical, but normal sensation with impaired higher sensory processing, such as graphesthesia and stereognosis in cortical
- Visual dysfunction: visual field cuts in subcortical, usually not in cortical (unless lesion in occiput)
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