Reversible Decerebrate Posturing Secondary to Hypoglycemia

DONALD G. SEIBERT, M.D.

Fairmont, West Virginia

Two cases of decerebrate posturing that resolved following the administration of dextrose are reported. The literature on hypogly cemia-induced neurologic deficits is reviewed and an explanation for the quick remission of the decerebrate posturing ‘is postu- lated.

Hypoglycemia may present with altered cortical or subcortical function. This may range from lightheadedness to confusion, seizures [ 11, or coma [2], Diplopia, hemiplegia [3], clonus, extensor plantq reflexes [ 21, and late development of a prolonged neuropathy, paresis [4], and decorticate posturing [5, 61 have been reported. There have been, however, no previous reports of reversible decerebrate posturing secondary to hypoglycemia.

CASE REPORTS

From the Fairmont General Hospital, Fairmont, West Virginia. Requests for reprints should be addressed to Dr. Donald G. Seibert, 106 Citadel Road, Morgantown, West Virginia 26505. Manu- script accepted May 4, 1984.

Patient 1. A 70-year-old woman was brought to the emergency department from a local nursing home with coma and decerebrate posturing. She had chronic renal failure, a prior myocardial infarction, recent left hip surgery, and adult-onset diabetes mellitus. Her medications included digoxin 0.125 mg every other day, furosemide 40 mg every other day, cimetidine 300 mg twice a day, and NPH U-100 insulin 15 units every morning. She had no previous history of a hypoglycemic episode. In the early morning, she was found diaphoretic and unresponsive to stimuli. She was afebrile, had a pulse of 62 beats per minute, respiratory rate of 26 per minute, and a blood pressure of 160/100 mm Hg. Noxious stimuli resulted in bilateral arm and leg extension with bilateral forearm pronation. Attempts to move an extremity or apply painful stimuli to an extremity resulted in increased motor tone of that ex- tremity but no purposeful withdrawal movements. There was an occasional repetitive contraction of the right elbow flexors. Pupils were equal and re- active to light. Results of the remainder of her physical and neurologic ex- aminations were normal. Her glucose level was 35 mg/dl. Her white blood cell count was 13.9 X 10g/liter, hematocrit 39.6 percent, blood urea nitrogen 95 mg/dl, creatinine 4.2 mg/dl, sodium 129 meq/liter, potassium 4.7 meq/ liter, chloride 93 meq/liter, and her digoxin level was 3.4 rig/ml. On pre- sentation, she received 50 ml of 50 percent dextrose and became alert and conversant. Fifteen minutes later, she again became obtunded and again received 25 g of dextrose. The decerebrate rigidity did not reoccur. She was admitted for monitoring and insulin dose regulation. Patient 2. A 59-year-old man presented to the emergency department with coma and decerebrate posturing. The patient had a history of chronic ob- structive pulmonary disease and had been prescribed terbutaline sulfate 5 mg three time a day. He had a history of a 30-pound weight loss over the last two years and chronic ethanol abuse. One day after checking into a local motel, he was discovered lying obtunded on the floor. The motel clerk at-

1096 June 1995 The American Journal ol Medlclne Volume 79

HYPOGLYCEMIA-INDUCED DECEREBRATE POSTURING-SEIBERT

tempted to arouse the man, who responded with some arm waving and some unintelligible commentary. His room was searched, disclosing four 1.5ounce whiskey sampler bottles. The patient was rechecked periodically by the clerk and was noted to be getting progressively more obtunded. He was then transported to the emergency department via ambulance.

His temperature was 95.8’F, pulse 180 beats per minute, respiratory rate 18 per minute, and his blood pressure 140/90 mm Hg. He was diaphoretic and comatose. Painful stimuli resulted in hyperextension of upper and lower extremities with bilateral arm pronation. His pupils were anisocoric. There were no spontaneous extremity motor movements. Reflexes were brisk and symmetric. There were bilateral extensor plantar reflexes and ankle clonus. The patient initially was believed to have an expanding supratentorial lesion. He un- derwent intubation and hyperventilation and received a IO mg bolus of dexamethasone. Plans were made for his transport to a neurosurgical facility. Following the dexa- methasone, he received a 25 g bolus of dextrose. He im- mediately awoke and performed extubation himself. The extensor plantar reflexes, clonus, and decerebrate posturing had resolved, although the pupils remained anisocoric for several hours. He received another bolus (12.5 g) of dextrose. The blood glucose level obtained after this bolus was 355 mg/dl. He subsequently had two fasting blood glucose levels of 94 and 97 mg/dl. No studies were made on longer fasts or with concomitant insulin levels. Because of his weight loss, an extensive occult malignancy work-up was undertaken but was unrevealing.

COMMENTS

The presentation of coma and decerebrate rigidity in both patients was complicated by anisocoria, clonus, and bilateral plantar reflexes in Patient 2. This resolved with the administration of dextrose. Other authors have reported reversible focal neurologic deficits secondary to hypoglycemia. Mahler et al [3] described one patient with readily reversed diplopia, anisocoria, extensor plantar reflexes, and hemiplegia. Silas et al [7] de- scribed a patient with a dense hemiplegia that re- solved within fw minutes of dextrose administration.

Other neurologic findings may not be readily re- versible. Paresthesias leading to muscle weakness and wasting [8] and paresis [4] may result in a slowly healing chronic deficit. Kalimo and Olsson [2] reported a case in which the extensor plantar reflexes were normalized with dextrose administration, yet the patient remained in a three-month coma and then died. Pro- longed coma, with evolution of major central nervous system lesions, has later led to decorticate posturing [5,61.

The differentiation of whether a focal neurologic finding is reversible or not may well be secondary to the extent of neuronal damage with hypoglycemia. This may range from a normal specimen to an extensive necro- tizing injury [2,5].

Similar to the patients in this report, three patients with hepatic coma and either decerebrate or decorticate posturing were described by Conomy and Swash [9]. Each patient had a rapid onset of coma, with posturing that resolved along with the coma in two to three days. The two patients that were decerebrate similarly had clonus and extensor plantar reflexes. The rate of res- olution was much slower in these patients than in Pa- tients 1 and 2 in the current report. This may have been due to the inherently more prolonged course of a he- patic coma.

Decerebrate rigidity is usually secondary to a su- pratentorial lesion, although, in addition to hepatic failure, central nervous system infection and cerebral anoxia may also be the cause of the rigidity [lo]. Similar posturing may also be due to a tonic seizure. Kinnier Wilson [ 1 l] reported two cases and summa- rized three previously reported cases of decerebrate posturing secondary to a tonic fit. In that report, deo- erebrate rigidity resolved with cessation of the seizure activity. It is proposed that the reversible decerebrate posturing of the two patients in this report was secon- dary to hypoglycemia-induced tonic seizure activity.

REFERENCES

1. Runge TM, Gilbert JT, Pelphrey CF: lnsulinoma simulating 6. Liebaldl Gp, Schleip I: Aphallic syndrome following protracted epilepsy. Neurology 1957; 7: 870-872. hypoglycemia. Monogr Gesamtgeb Psychiitr (Berlin) 1977;

2. Kalimo H, Olsson Y: Effects of severe hypoglycemia on the 14: 37-43. human brain. Acta Neurol Stand 1980; 62: 345-358. 7. Silas JH, Grant DS, Maddocks JL: Transient hemiparetic at-

3. Mahler RJ, Grann V, Purr& R: Functioning islet cell adenoma. tacks due to unrecognized nocturnal hypoglycemia. Br Med JAMA 1964; 168: 791-793. J 1981; 282: 132-133.

4. Silfverskiokl BP: Polyneuritis hypoglycemia-late peripheral 8. Mulder DW, Bastron JA, Lamberl EH: Hyperinsulin neurono- paresis after hypoglycemic attacks in two insulinoma pa- pathy. Neurology 1956; 6: 627-635. tients. Acta Med Stand 1946; 125: 502-504. 9. Conomy JP. Swash M: Reversible decerebrate and decorticate

5. Langauer-Lewowicka H, Zuchowska B, Zajac-Nedza M: postures in hepatic coma. N Engl J Med 1988; 278: Zaburzenia czynnosci bioelektrycznej mozgu w ostrych 878-879. zatruciach srodkami hipoglikemizujacymi (cerebral bios 10. Davis RA, Davis L: Decerebrate rigidity in humans. Neuro- lectric activity disorders in acute intoxication with hypo- surgery 1982; 10: 635-642. glycemic agents). Neurol Neurochir Pol 1979; 13: 147- 11. Kinnier Wilson SA: On decerebrate rigidity in man and the 153. occurrence of tonic fits. Brain 1920; 43: 220-268.

June 1985 The American Journal ol Medlclne Volume 78 1037