Approach to weakness and sensory loss

Question 1

Approach to weakness

Answer 1

• Distinquish true muscle wealness from lack of energy or motor impairment not due to loss of muscle power.
  
  • i.e., is patient actually obectively weak when muscle strength is formally tested? Can also ask if patient is “weak” or if they are unable to perform certain tasks (ex. comb hair)- the ladder is a true muscle weakness.
• Localizing the site of the lesion producing the weakness
  
  • Distribution of weakness:
    
    • Generalized weakness - some cases of myasthenia gravis, cachexia, periodic paralysis
    • Asymmetric weakness - central or peripheral nervous system
    • Symmetric
      
      • Distal - reduced grip stretch, weakness of wrist flexion/extension, weakness of plantar flexion, foot drop. Early motor neruon disease or peripheral neuropathy.
      • Proximal - weak neck flexion/extension, weak deltoids and hip flexors. Myopathy, muscular dystrophies, and myasthenia gravis.

Question 2

Clinical Investigations for Muscle weakness

Answer 2

• Elevations of plasma muscle enzymes (creatin kinase, aldolase, lactate dehydrogenase, and aminotransfersase) are suggestive of muscle disease.
• Serologic tests - antinuclear antibodies, antibodies against nuclear antigens and myositis specific antigens can help determine if there is an inflammatory myopathy or associated connective tissue disease.
• Electrophysiologic studies - nerve conduction and EMG is lesion is suspected to be in peripheral nervous system, neuromuscular junction, or muscle itself.
• MRI - useful for selecting muscle for biopsy
• Genetic testing - useful to confirm diagnosis and categorize patients with muscular dystrophies and heritable myopathies.

Question 3

Sensory crossing

Answer 3

• Pain, temp, and touch - enter spinal cord via dorsal nerve root. They synapse with second order neurons in dorsal horn and then cross the midline of the cord. Second order neurons now ascend on the opposite side of the spinal cord to the peripheral nerve in either anterior spinothalamic tract (touch) or lateral spinothalamic tract (pain and temperature) to the thalamus where they synapse with neruons that ascend to primary sensory cortex in parietal lobe.
• Proprioceptive, vibratory, pressure, and touch enter the dorsal colums directly from the dorsal root, which synpase which synpase with second order neruons in cuneate and gracile nuclei of medulla. These second order neurons cross midline of medulla and ascend through brainstem to the thalamus where they synpase with 3rd order neurons to parietal lobe.

Question 4

Patterns of Sensory Loss

Answer 4

• Sensory loss confirmed to part of a limb = injury to peripheral nerve, nerve plexus, or spinal root.
• Sensory loss involving most of an extremity or to the trunk indicates presence of another disorder that can be distinquished as follows:
  
  • Both sides of the body= polyneuropathy or spinal cord idsease
  • One side of the body = contralateral disease of the brainstem, thalamus, or cerebral hemispheres.
    
    • Sensory loss of face on same side of the body = upper brainstem, thalamic, or hemispheric disease
    • Sensory loss of face on opposite side as body = lower brainstem
  • Stocking-glove sensory loss = axonal neuropathies
  • Disproportionate loss of vibration sense and proprioception compared with pain and temp = dorsal colums of spinal cord and demyelinating polyneuropathy.

Question 5

Neuropathy

Answer 5

Mononeuropathy and radiculopathy

• Mononeuropathy - pathology affecting individual peripherial nerve. Signs and symptoms correlate with individual nerve distribution (ex. carpal tunnel syndrome).
• Radiculopathies - pathology affecting the nerve root. Signs and symptoms correlate to the dermatome and myotome. Due to overlap in nerve root innervation of muscles and dermatomes, weakness and sensory loss can be mild and/or not involve the entire region. Characteristically result in a severe lancinating pain that may be exacerbated by coughing, sneezing, or straining.

Question 6

Distal Sensory Polyneuropathy

Answer 6

• Stocking-glove sensory loss. Usually due to:
  
  • Diabetes, alcohol, vitamin B₁₂ deficiency, syphilis, HIV, Lyme disease, uremia, chemotherapy, vasculitis, paraneoplastic neuropathy, amyloidosis.
• In axonal neuropathies, longest axons are affected first - symptoms start distally and progress proximally.

Question 7

Sensory Neuronopathies

Answer 7

• Rare causes of sensory loss. Due to degeration at level of dorsal root ganglion. Manifest with sensory ataxia, absent reflexes, and dysesthesias, as well as sensory loss.
  
  • Tend to be asymmetric
  • Lack of motor involvement
  • Causes - Sjogrena, Guillain-Barre, Chemotherapy induced, Vitamin B₆ toxicity, Friedreich ataxia.

Question 8

Spinal Cord Lesions

Answer 8

• Syringomyelia/cape distribution sensory loss - due to lesions of central cervical cord. Loss or reduction of sensation for pinprick and temperature across upper back, shoulder, and upper arms.
• Brown-Sequard syndrome - results from lesion on only one side of the spinal cord. Patients presents with reduced proprioception, vibration, and weakness on ipsilateral side, and decreased pinprick and temperature on contralateral side.

Question 9

Brainstem Lesions

Answer 9

• Most brainstem lesions involve cranial nerves and/or their nuclei
• Pain and temperature loss on ipsilateral face and contralateral limbs and trunks.

Question 10

Thalamic lesion

Answer 10

• Contralateral sensory deficit involving all sensory modalities to varying degrees.

Question 11

Sensory Cortex

Answer 11

• Discrete lesions of sensory cortex are rare. When they occur they affect part of the body that corresponds to the homunculus.