A 26-year-old woman comes to the emergency department due to numbness and weakness of both legs. Throughout the prior day, the patient felt as if her legs kept "going to sleep," and on waking this morning, she had difficulty standing and walking. She also reports urinary urgency and 2 episodes of involuntary urine leakage. The patient has no history of back pain or trauma. Four years ago, she was diagnosed with type 1 diabetes mellitus, and her glycemic control is maintained by a continuous subcutaneous insulin infusion pump. Temperature is 36.9 C (98.4 F), blood pressure is 134/78 mm Hg, and pulse is 76/min. Visual acuity, pupillary reflexes, and funduscopy are normal. Muscle strength in the right and left lower extremities are 3/5 and 4/5, respectively. Patellar reflexes are 3+ on both sides, and plantar reflexes are upgoing. Sensation to vibration, light touch, and pain is decreased in both legs. There is decreased sensation on left side of the face. Fingerstick glucose level is 144 mg/dL. What is the most likely diagnosis in this patient?
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This patient has rapidly progressive weakness with upper motor neuron signs (hyperreflexia, upgoing Babinski), sensation deficits with a localizing spinal sensory level, and bladder dysfunction, consistent with transverse myelitis. She also has another neurologic deficit that may localize to the brainstem (numbness of the face). In a woman of childbearing age, this is highly suspicious for the first presentation of multiple sclerosis. A confirmed diagnosis requires deficits that are disseminated in:
This patient has neurologic deficits disseminated in space, but it is unclear whether they are disseminated in time. Therefore, past medical conditions should be reviewed for suspicious neurologic symptoms (eg, facial numbness) that may represent a previous attack. In addition, MRI can prove dissemination in time by revealing old lesions. Lumbar puncture can show oligoclonal bands, which can indicate ongoing inflammation. If nothing confirms dissemination in time, close follow-up may reveal new attacks or lesions.
(Choice A) Diabetic polyneuropathy causes symmetric sensory loss in a stocking-glove distribution. It occurs insidiously, approximately 5 years after a diagnosis of type 1 diabetes mellitus. Motor deficits occur months to years later than sensation deficits and would be associated with lower motor neuron signs (eg, hyporeflexia).
(Choice B) Guillain-Barré syndrome leads to rapidly progressive ascending muscle paralysis generally preceded by infection (eg, Campylobacter jejuni, viruses). However, it impacts lower motor neurons, so hyporeflexia (vs hyperreflexia) is expected.
(Choice D) Normal pressure hydrocephalus (NPH) can present with difficulty walking, urinary incontinence, and upper motor neuron signs. However, difficulty walking is due to ataxia (vs motor weakness); this patient lacks cognitive dysfunction (key feature of NPH), and idiopathic NPH is uncommon in women age <50. In addition, this patient's facial numbness, sensory symptoms with a distinct spinal level, and young age make MS more likely.
(Choice E) A symptomatic parasagittal meningioma could cause numbness and weakness of the bilateral, symmetric lower limbs with upper motor neuron signs and urinary incontinence. However, these symptoms would be slowly progressive and would not explain facial numbness.
(Choice F) Long-standing vitamin B12 deficiency can cause subacute combined degeneration of the spinal cord, leading to progressive symmetric sensory loss/paresthesia, sensory ataxia, and spastic muscle weakness. Symptoms develop over weeks to months rather than days.
Educational objective:
Multiple sclerosis presents with neurologic deficits disseminated in space and time. Common initial presentations include transverse myelitis, optic neuritis, internuclear ophthalmoplegia, and cerebellar dysfunction. These initial presentations may not be disseminated in time, but further work-up and follow-up can confirm the diagnosis.