Leg Weakness, Presumed Seizure

Figure 1. (Please click to enlarge)

Figure 2. Page shot (Please click to enlarge)

History:  A 43-year-old man with a history of alcohol addiction is transported to the emergency department by ambulance for bilateral leg weakness following a presumed seizure. The patient is no longer post-ictal and states that unlike prior seizures from alcohol withdrawal, this time he was unable to walk normally after he woke up. He says the difficulty walking is due to weakness in both of his legs. He admits to some mild chronic back pain, which he reports is no different from its baseline. He denies any fever, neck, or leg pain or numbness, headache, bowel or bladder problems, vomiting, or other complaints.

Examination: Vital signs show a temperature of 98.9°F, BP 162/93 mm Hg, and pulse of 112 beats/min. He has no spinal tenderness and his straight leg raise test is normal bilaterally. On strength exam he is 4-/5 in both legs and 5-/5 in both arms. He is also noted to have brisk deep tendon reflexes (DTRs), especially considering his chronic alcohol use, which is known to be associated with decreased DTRs.

Laboratory values:  K = 3.3 mEq/L; Na = 146 mEq/L; Hb = 10 g/dL. Other basic lab results are unremarkable.

Initial concern(s): Electrolyte abnormality, spinal cord compression, stroke, trauma

QUESTION:

What additional testing should be ordered?

For answer and discussion, please click “next” below.

ANSWER:

What additional testing should be ordered? Magnesium, phosphorus, head CT, and an ECG.

Rationale: Head CT should be ordered after an alcohol withdrawal seizure, even in the absence of trauma. Intrahemispheric subdural hemorrhage can cause bilateral leg weakness.

Fortunately the head CT was normal, but the patient’s magnesium level was low (0.7 mg/dL). It was rechecked and confirmed. The ECG tracing (Figure 1 at right; please click on image to enlarge) surprisingly shows a normal QT interval.

Discussion
Hypomagnesemia is an uncommon electrolyte abnormality that is often asymptomatic, but may present with paresthesia, weakness, tremor, and muscle cramps. Less common presentations include altered mental status, tetany, seizures, or GI upset. Renal causes of hypomagnesemia include losses from diuretics, hypercalcemia, renal wasting, or Conn’s or Bartter’s syndrome. GI causes include diarrhea or malnutrition, most commonly from alcoholism. Medications can also contribute to hypomagnesemia.

Abnormal exam findings are rare and are listed in Figure 2 at right (please click on page shot to enlarge). ECG abnormalities may occur as well, the most common being prolongation of the QT interval. Other ECG irregularities seen include T-wave abnormalities and atrial and ventricular extra beats and dysrhythmias. The diagnosis of hypomagnesemia is typically from serum electrolyte testing.

Treatment for hypomagnesemia is with repletion either by mouth or IV. IV repletion is usually recommended if there are ECG abnormalities, the patient is experiencing symptoms or is being admitted to the hospital. It is important to note that only about 1% of total body magnesium is serum, so repletion of total body stores may take days (click on page shot in Figure 2 to the right for more information and to enlarge).

Case outcome: CT brain and lumbar spine showed nothing acute. With magnesium repletion the weakness gradually resolved. It is unclear in this case why the weakness in both legs only occurred after the seizure and not before when the magnesium level was likely similar.