CASE REPORT Reversible decerebrate posturing after profound and prolonged hypoglycemia MALCOLM M. KIRK, MD; BYRON J. HOOGWERF, MD; JAMES K. STOLLER, MD • Decerebrate rigidity is one of several reversible neurological abnormalities which have been observed in the setting of metabolic coma. We present the case of a patient who recovered fully from prolonged decerebrate rigidity associated with hypoglycemic coma. This case emphasizes the possibility of recovery from severe, prolonged hypoglycemia. • INDEX TERMS: DECEREBRATE RIGIDITY; HYPOGLYCEMIC COMA; REVERSIBLE POSTURING • CLEVE CLIN ] MED 1991; 58:361-363 YPOGLYCEMIA may cause a number of results included: serum glucose 8 mg/dL, potassium 7.7 changes in brain function, some of which mEq/L, sodium 144 mEq/L, BUN 146 mg/dl, bilirubin are reversible. We describe the case of a 0.5 mg/dl, and serum pH 6.98. With initial correction patient who recovered after exhibiting of acidemia and hypoglycemia (3 ampules of 50% Hdecerebrate posturing for six hours during hypo- dextrose over one hour), serum glucose rose to 224 glycemia from a massive insulin overdose. mg/dl and decerebrate posturing ceased. One hour later, however, unresponsiveness with decerebrate pos- CASE REPORT turing recurred. Serum glucose was found to be less than 20 mg/dl, and he was transferred to the Cleveland A 32-year-old man with poorly controlled type I Clinic Hospital. diabetes mellitus of 19 years' duration complicated by On arrival, about 6 hours after the initial presenta- end stage renal disease and peripheral and autonomic tion, he was unresponsive and diaphoretic with roving neuropathy, was found unresponsive in his home. He eye movements. His temperature was 38.6°C (axil- had a history of frequent hypoglycemic episodes, in- lary), blood pressure was 132/80, heart rate was 160 cluding several in the five days before presentation. and regular, and respirations were 32. Sternal pressure On initial presentation to a local hospital emergen- elicited decorticate posturing. Bilateral corneal cy room, the patient was bradycardic (40 beats/min) reflexes were present, and the patient moved all ex- and hypotensive. He was treated with intravenous tremities spontaneously. Deep tendon reflexes were ab- atropine within three minutes of arrival, after which he sent, but plantar reflexes were extensor bilaterally. assumed a decerebrate posture. Noteworthy laboratory Two hours after admission, the patient had a brief tonic-clonic seizure. Serum glucose was 26 mg/dL at From the Departments of Pulmonary Disease (M.M.K.J.K.S.), the onset of the seizure. A residual decerebrate posture and Endocrinology (B.J.H.), The Cleveland Clinic Foundation. remained for the next 6 hours, during which time his Address reprint requests to M.M.K., Department of Medicine, serum glucose level remained less than 60 mg/dL in The University Hospitals of Cleveland, 2074 Abington Road, spite of 100 mg of intravenous methylprednisolone, Cleveland, Ohio 44106-5000. JULY • AUGUST 199Downloaded1 from www.ccjm.org on October 3, 2021. For personal use only. All otherCLEVELAN uses requireD CLINI permission.C JOURNAL OF MEDICINE 361 REVERSIBLE DECEREBRATE POSTURING • KIRK AND ASSOCIATES and a total of 800 mL of 50% dextrose solution. rapidly resolved when hypoglycemia was corrected and When the serum glucose level rose to 238 mg/L and recurred when hypoglycemia returned. was maintained at roughly this level, decerebrate pos- Two previous cases of reversible decerebrate postur- turing disappeared, and the patient's level of conscious- ing secondary to hypoglycemia have been reported. ness progressively improved. Over the next 3 days, Seibert8 described the remission of decerebrate postur- serum glucose levels ranged from 130 mg/dL to 250 ing after administration of intravenous glucose in two mg/dL, and his mental status returned to a reported patients, one of whom was a man with adult-onset baseline of verbal coherence, alertness, answering yes diabetes who presented in coma with decerebrate pos- or no questions, and following simple commands. turing in response to painful stimuli and a serum Decerebrate posturing did not return once the glucose of 35 mg/dL. He became alert and conversant hypoglycemia was corrected. following 50 mL of 50% dextrose. (The other patient This patient's prior episodes of sustained was a 59-year-old male alcoholic with neither diabetes hypoglycemia, and the severe degree and long duration nor insulinoma and without documented hypo- of the current hypoglycemic episode were consistent glycemia, who presented with hypothermia, tachycar- with an insulin overdose. This was confirmed by a dia, diaphoresis, and coma with decerebrate posturing, serum insulin concentration of greater than 11,000 as well as anisocoria and bilateral extensor plantar |aU/mL (normal fasting concentration 4 to 24 (lU/mL) reflexes. He awoke and became neurologically normal in a sample obtained 12 hours after his initial presenta- immediately after receiving 25 g of dextrose.) tion to the local hospital. At 96 hours after presenta- The second case, described by Ogunyemi and tion, the level was 79.7 pU/mL, and at 108 hours, it Olowoyeye,9 concerned a 65-year-old man with was 65.0 |0.U/mL. Assays for plasma protein binding of hypoglycemia caused by religious fasting and diarrhea. insulin ("insulin antibodies") showed <5% binding, He became comatose with decorticate posturing on the which is considered to be a normal value and of no right side in response to painful stimuli on either side of clinical significance in patients with diabetes mellitus. the body. The serum glucose was 8 mg/dL. An in- travenous bolus of 100 mL of 50% dextrose solution DISCUSSION resulted in resolution of the decorticate posture and return of consciousness within 90 minutes. The current report demonstrates two uncommon Our patient's course differs from the previously but noteworthy clinical points: (1) decerebrate postur- described experience, principally in the duration of the ing in hypoglycemia may be transient and reversible decerebrate posturing. In each previous case, the com- with correction of hypoglycemia, and (2) neurologic atose patient demonstrated decerebrate posturing in recovery is possible despite severe insulin overdose response to painful stimuli, but decerebration was with prolonged hypoglycemia. rapidly reversed and consciousness restored by a single Abnormal posturing was first observed in ex- dose of dextrose. In the current case, posturing oc- perimental animals following intercollicular section of curred intermittently for 6 hours after admission, then the brain stem (decerebrate)1'2 and removal of all cor- constantly for 6 hours, and the presence of decerebrate tex and white matter above the level of the basal rigidity coincided with hypoglycemia. ganglia (decorticate). These two postures have been It is known that hypoglycemia can cause seizures, consistently produced by specific anatomic lesions in and Seibert8 postulated hypoglycemia-induced tonic experimental animals, and it has been inferred that seizure activity as a mechanism for the decerebrate analogous anatomic lesions are responsible for these rigidity seen in his patients. Our patient, however, postures in humans. Indeed, clinical decortication and clearly demonstrated adduction, extension, and prona- decerebration most often result from a structural lesion tion of the arms, a posture very different from the (usually trauma). However, a variety of metabolic and abduction and flexion of the arms seen in global tonic other causes have been reported, including anoxia,3 seizures.10 Furthermore, this patient's posture was made infections,4 hepatic coma,5,6 the syndrome of inap- more prominent by noxious stimuli, which is typical of propriate secretion of antidiuretic hormone (SIADH),7 decerebrate rigidity11 but not of seizures. Haines12 and hypoglycemia.8,9 A few of these non-structural describes five cases of decerebrate posturing which causes have been associated with reversible posturing. were misinterpreted as seizures, and gives an excellent In our patient, decerebrate rigidity coincided with account of the manner and importance of differentiat- hypoglycemia. During the first 6 hours, decerebration ing between the two. 362 CLEVELAND CLINIDownloadedC JOURNAL fromOF MEDICIN www.ccjm.orgE on October 3, 2021. For personal use only. All other uses require permission.VOLUME 58 NUMBER 4 REVERSIBLE DECEREBRATE POSTURING • KIRK AND ASSOCIATES Our patient's return to baseline neurologic status can be inferred from the serum insulin level: 12 hours after a total of more than 6 hours of decerebration was after admission it exceeded 11,000 (¿U/mL, which is unexpected. Arem and Zoghbi13 indicate that full among the highest values ever reported. However, con- neurologic recovery after prolonged hypoglycemic founding factors make it difficult to estimate the size of coma without posturing (up to 6 days) is not unusual, the dose. When injected intravenously, insulin has a although there is no account of recovery from such plasma half-life of about 10 minutes,14 but the principal prolonged hypoglycemic decerebration. Using a determinant of serum levels is the rate of release from pooled analysis of eight of their own patients and 38 the injection site which, in turn, is influenced by the cases from the literature, Arem and Zoghbi found that type of insulin used. An added factor in this case was neither the magnitude of the insulin dose nor the the presence of complete renal failure, a variable not severity of the