What are the physical exam findings in patients with CNS lupus?

Updated: May 04, 2021
  • Author: Pradeep C Bollu, MD; Chief Editor: Niranjan N Singh, MBBS, MD, DM, FAHS, FAANEM  more...
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Answer

Abrupt or subacute onset of any focal neurologic deficit in systemic lupus erythematosus (SLE) may result from local vasculitis with thrombosis, distant artery-to-artery embolization, or cardiac emboli. Mass lesions (e.g., subdural or parenchymal hemorrhages) or brain abscess remain in the differential diagnosis.

Paraparesis implicates cauda equina, thoracic-lumbar spinal cord, partial lesions of the cervical cord, brainstem lesions, or parasagittal cerebral lesions. Extensor toe signs localize to the cord or above, excluding cauda equina. Acute lesions at either cauda or cord levels may be associated with hyporeflexia, areflexia, or sphincter disturbances. If an areflexic paraparesis is unaccompanied by a sensory level or spreads to the arms, acute demyelinating polyneuropathy (Guillain-Barré syndrome) should be considered. Sensory loss to pain and temperature with sparing of posterior column function (position sense, graphesthesia with or without vibration sense) suggests an anterior spinal artery syndrome.

Clinically involved cord levels require immediate imaging (ie, myelography or magnetic resonance imaging [MRI]) to exclude compressive lesions. If myelography is performed, spinal fluid should be collected for analysis before introducing contrast media.

Cranial neuropathies most commonly result from lupus vasculitis affecting the vasa nervorum supplying the involved nerve. Although optic neuritis (painful or painless subacute loss of visual acuity, usually accompanied by visible inflammation of the optic nerve head) and retrobulbar neuritis are most common, any cranial nerve may be affected. Imaging studies can exclude compressive lesions that result from opportunistic infection, tumor, or aneurysm.

Diffuse weakness may result from polyneuropathy, myopathy, neuromuscular junction disease, or systemic fatigue.

Examination findings of objective, symmetric proximal muscle weakness (with or without concomitant pain) support myopathy, whereas distal symmetric weakness (with distal sensory loss) implicates a peripheral polyneuropathy. Myopathy should never be accompanied by sensory loss, but it may at times be asymmetric.

Mononeuritis multiplex results in patchy, asymmetric weakness, sensory loss, or both in the distribution of multiple peripheral nerves or roots. Clinical distinction between proximal myopathy and polyradiculopathy or proximal mononeuritis multiplex may be difficult, requiring electromyogram (EMG) or nerve conduction velocity (NCV) studies or even nerve and muscle biopsies for an accurate diagnosis.

Weakness that improves or worsens with repetitive testing suggests a neuromuscular junction defect. Painful give way weakness without organic muscle weakness supports arthralgia or other musculoskeletal etiology.

Fatigue from autoimmune disorder is rarely accompanied by objective muscular weakness. Orthostatic hypotension should be excluded.


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