Alternating transient dense hemiplegia due to episodes of hypoglycemia

ACUTE ONSET OF HEMIPLEGIA is a common presentation of cerebrovascular accident. Rapid reversal of this focal neurologic deficit may occur with transient ischemic attacks. However, hypoglycemia has been reported only rarely as a cause of reversible motor deficits. We now report the first case of a patient with alternating right and left dense hemiplegia related to episodes of hypoglycemia.

Report of a Case
A 69-year-old African American male with a medical history, congestive, chronic renal insufficiency, anemia, and myocardial infarction in 1988, was diagnosed as having type II diabetes mellitus. One week prior to admission, he was started on glyburide5 mg orally once a day. There was no prior history of cerebrovascular insufficiency, headache, or seizure disorder. His family history was noncontributory.

Approximately 18 hours prior to admission, the patient developed gradually worsening slurring of speech and right-sided motor weakness. He initially ignored these symptoms, but on waking up the following morning, he was unable to move the right side of his body. There was no history of nausea, vomiting, headache, trauma to the head or body, chest pains, fever, chills, shortness of breath, or seizure activity associated with this episode. The patient previously had been independent in his daily activities and lived alone without assistance. He drank alcohol socially, but he had stopped smoking eight years before and denied other substance abuse. Medications upon admission were: aspirin 325 mg daily, isosorbide dinitrate 10 mg three times a day, digoxin 0.125 mg daily, furosemide 40 mg daily, hydralazine 25 mg three times a day, and the glyburide.

In the emergency room, the patient was alert, oriented, and cooperative with examiners. His speech was slurred, and he was unable to move the right side of his body. Vital signs were: blood pressure 192/88 mm Hg (left arm, supine, without orthostasis); heart rate 85 beats per minute and regular; respiratory rate 22 per minute and unlabored; and temperature 96.8°F. Pulse oximetry revealed an oxygen saturation of 98%, and a fmgerstick blood glucose determination was 1.39 mmol/liter (25 mg/dl). The patient was pale and had trace ankle edema bilaterally. His cardiovascular examination was notable for a soft, systolic murmur along the left sternal border and bilateral femoral bruits. There were no carotid bruits. Chest and abdominal examination findings were normal. On neurological examination, his speech was slurred but intelligible, there was right facial weakness, his upper and lower extremity motor strength was 0 of 5 on the right, and his right toe was up-going. The remainder of his cranial nerve examination and sensory and cerebellar function tests were within normal limits.

Laboratory data were: hemoglobin 1.02 mmol/liter, hematocrit. 0.197, mean corpuscular volume 90 fl, white blood cell count 8,100/ul, platelets 200,000/ul, reticulocyte count 0.8%, prothrombin time and partial thromboplastin time within normal limits; urea nitrogen 22.5 mmol urea/liter, creatine 531 umol/liter, sodium 143 mmol/liter, potassium 4.7 mmol/liter, chloride 120 mmol/liter, bicarbonate 16.2 mmol/liter, anion gap 7 mmol/liter, glucose 1.66 mmol/liter (30 mg/dl), calcium 2.2 mmol/liter, phosphate 1.2 mmol/liter. His liver function tests were within normal limits, but a creatine phos-phokinase (CPK) was elevated at 686 U/liter. A digoxin level was 0.62 nmol/liter. Head computerized tomographic (CT) scan did not reveal any abnormalities.

The patient was given two 50-ml ampules of 50% dextrose in water intravenously, and his speech and right-sided motor function returned to normal within 10 minutes. generic Levofloxacin online

Following admission, the patient was monitored with telemetry and frequent vital sign determinations. He was given intravenous 5% dextrose in 0.5% saline. Subsequent glucose determinations were in the range of 2.22-5 mmol/liter (40-90 mg/dl). Acute myocardial infarction was excluded by serial cardiac enzyme determinations. After six hours of hospitalization, the patient again developed slurred speech and manifested hemiplegia, this time involving the left side of his body. This episode occurred in the presence of a physician, and a detailed neurologic examination at that time confirmed left facial weakness and dense left hemiplegia. Motor strength was normal on the right side during the second episode. The patient’s vital signs were stable, but a fmgerstick determination again revealed hypoglycemia with a glucose level of 1.89 mmol/liter (34 mg/dl). Two 50-ml ampules of 50% dextrose in water were administered, and the speech and left-sided neurologic deficit resolved before the second ampule was completely infused. Cardiac telemetry remained normal during the episode. A repeat CT scan of the patient’s head was normal as were Doppler studies of his carotid blood flow. The patient subsequently remained asymptomatic and was discharged on his regular medications, except gly-buride, to follow up with his primary care physician.

Hypoglycemia may result in two categories of symptoms, adrenergic and central nervous system. The former include pallor, sweating, tremors, tachycardia, hunger, and anxiety. Central nervous system symptoms, also called “neuroglycopenia,” include headache, dizziness, visual problems, confusion, erratic behavior, convulsions, and loss of consciousness. Motor dysfunction is rarely seen. There can be a stereotypic subset of symptoms with repeated events. None of the above-mentioned symptoms are specific for hypoglycemia, and a broad differential of structural and metabolic etiologic factors exists. omnicef 300

Adrenergic symptoms are usually evident when blood glucose rapidly falls to a low level. This circumstance, however, may not happen in patients with longstanding diabetes. Gradual decline of blood glucose to hypoglycemic levels is also more likely to result in central nervous system dysfunction without an adrenergic component.

Many studies in healthy individuals have defined the sequence of events that accompany an insulin infusion and fall in glucose level. Neurologic symptoms generally develop at blood glucose levels below 2.5 mmoHiter (45 mg/dl), and major dysfunction may be expected below 1.1 mmol/liter (20 mg/dl). In diabetics, considerable variation may be seen depending on chronicity of the disease and prior control of blood sugar component.

Reversible or irreversible hemiparesis is a recognized but rare symptom of neuroglycopenia. A clinical review of 29 documented cases by Forster and Hart indicated that 75% of patients were on insulin and 14% were on oral agents for blood glucose control. Right hemiparesis was more common than left-sided involvement. Episodes could reoccur on the same side and last for a few hours or even days. An elderly population with a previous history of cerebrovascular accident was more likely to be afflicted. generic atomoxetine

The mechanism of hypoglycemic hemiplegia has not been well-documented. The brain is a highly metabolic organ, which uses glucose as its exclusive energy source. Under hypoglycemic conditions, the energy demand is met by oxidation of cerebral lipids and proteins and may result in brain damage. Several theories may explain the pathogenesis of a hypoglycemia-associated motor deficit. Structural narrowing of blood vessels that supply a particular portion of the brain could result in even lower levels of glucose during generalized hypogly cemia. Angiographic studies, however, have failed to support this theory. Hypoglycemia may act on a cerebral vasomotor center to cause vasospasm in the smaller cortical vessels. A third theory attributes local vulnerability to hypoglycemia to differences in cellular metabolism and vascular supply. Both clinical and anatomic studies have demonstrated this theory, but the studies do not completely explain the phenomenon.

In the case presented, hypoglycemia was likely the result of an exaggerated effect of glyburide due to diminished renal clearance. The patient’s central nervous system deficits were rapidly reversible by the administration of intravenous glucose. Results of carotid Doppler studies and two computerized tomograms of his head were negative for structural lesions. Finally, alter nation of the side of the body involved in two closely occurring episodes of hypoglycemia suggest that vascular spasm and/or differences in local metabolism rather than fixed anatomic lesions may have played a role in our patient’s symptoms. buy imitrex online

We conclude that hypoglycemia should be considered in the differential diagnosis of any patient presenting with a change in mental status or central nervous system deficits. This includes patients with significant focal neurologic deficits such as hemiparesis/hemiplegia, which would generally be considered signs of cerebrovascular compromise. As in the presented case, hypoglycemia and its sequelae may be rapidly reversed if diagnosed early. Awareness of the possibility of hypoglycemia may be extremely important in diagnosing patients who are unable to provide any medical history upon initial encounter.

If hypoglycemia is suspected as the cause of neurologic deficits, 10-20 ml of blood should be drawn beyond that needed for glucose determination and routine investigations. Additional analysis, including insulin, C-peptide, Cortisol, and sulfonylurea levels, can then be determined as appropriate. Other tests, such as carotid Doppler studies, computed tomography, magnetic resonance imaging, or positron emission tomography of the head, or angiography, may be indicated for further evaluation.

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