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  IN THIS Article
 ::  Introduction
 ::  Case report
 ::  Discussion
 ::  Acknowledgments
 ::  References

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CASE REPORT
Year : 1990  |  Volume : 36  |  Issue : 4  |  Page : 227-9

Hypoglycemia masquerading as repeated focal stereotyped neurological deficit (a case report).


Department of Medicine, Seth G.S. Medical College, Parel, Bombay, Maharashtra.

Correspondence Address:
Department of Medicine, Seth G.S. Medical College, Parel, Bombay, Maharashtra.




How to cite this article:
Pathare A V, Kothari M A, Joshi V V, Chikhalikar A A, Dalvi S G. Hypoglycemia masquerading as repeated focal stereotyped neurological deficit (a case report). J Postgrad Med 1990;36:227


How to cite this URL:
Pathare A V, Kothari M A, Joshi V V, Chikhalikar A A, Dalvi S G. Hypoglycemia masquerading as repeated focal stereotyped neurological deficit (a case report). J Postgrad Med [serial online] 1990 [cited 2017 Dec 11];36:227. Available from: http://www.jpgmonline.com/text.asp?1990/36/4/227/822




  ::   Introduction Top

Under normal circumstances the circulating plasma glucose concentration is maintained within relatively narrow limits over the course of a 24-hour period. Hypoglycaemia is reduction in the plasma glucose concentration to levels, which are responsible for symptoms which generally revert upon restoration of a normal glucose concentration[4]. Hypoglycaemia therefore can be more readily defined in clinical rather than precise quantitative terms.
We are reporting a case of non-insulin dependent diabetes mellitus (NIDDM) on oral sulfonylurea derivative in whom, hypoglycaemia masqueraded as repeated, focal stercotyed neurological deficit. The unusual feature is that although hypoglycaemia affects all cerebral neurons, in our patient it produced repeated focal neurological deficit in the same vascular territory.

  ::   Case report Top

PGA, a 66-year-old male, a playwright by profession was admitted to the King Edward Memorial Hospital with a complaint of sudden onset of weakness of the right side of the body noticed immediately on rising in the morning. He was a right-handed person, with no prior history of hypertension or ischemic heart disease. However, he was a known diabetic (NIDDM) on regular treatment with oral sufonylurea derivative (Glybenclamide 5mg tid). On inquiry, he gave history of repeated episodes of transient ischemic attacks (TIAs) involving the right side of the body which used to clear off spontaneously especially after a cup of tea. He therefore did not seek any medical attention for the same until the present episode. There was no history suggestive of TIAs in any other vascular territory.
On examination, he was semiconscious lying supine with the right lower limb extended and externally rotated. He responded to painful stimulus by moving only the left side of his body. His pupils were central, circular, equal and reacted to light normally. Dolls eye movements were present in both directions and there was no suggestion of a conjugate gaze palsy on either side. He was febrile and his pulse was 102/min, regular. There was no evidence of any carotid bruit. His blood pressure in the right upper extremity was 130/90 mm of Hg in the supine position. Examination of his central nervous system revealed the presence of right supra-nuclear 7th cranial nerve palsy. Power in the right upper and lower extremity was grade zero on the MRC scale. He had a right hemi anaesthesia and homonymous hemianopia as evidenced by the menace reflex. Rest of the systemic examination was unremarkable. The patient was immediately given intravenous mannitol and low-molecular weight dextran in glucose in view of his typical features suggestive of a left middle cerebral artery (MCA) territory cerebrovascular accident. However, he showed a dramatic, complete improvement within an hour of institution of the above therapy, suggesting thereby a probable diagnosis of a TIA in the left MCA territory. Unfortunately, blood was not sent for any investigations prior to starting the therapy.
The patient was fine throughout that day and wanted discharge, but was persuaded to stay on for the sake of completing the investigations. However, next morning again he was found semiconscious, with weakness of the right side of the body. Motor examination revealed a power of grade zero on the MRC scale. Pupils were central, circular and equal with normal reaction to light. Dolls eye movements were normal in both the directions. He had a right hemi anaesthesia along with homonymous hemianopia as evidenced by the menace reflex. His pulse was 96/min and the blood pressure was normal. There was no evidence of neck stiffness. He was therefore immediately given intravenous glucose after having collected blood for sugar levels. He became alert within minutes receiving the intravenous glucose injection with complete disappearance of the weakness, thereby establishing the clinical diagnosis of hypoglycaemia. This was also simultaneously confirmed by the laboratory blood sugar estimations. His blood sugar was only 24mg% by the standard Folin-wu technique (normal values 80-120 mg%). He was immediately asked to discontinue the anti-diabetic medication.
His other investigations including blood urea, S. electrolytes, S. triglycerides and S. cholesterol were all normal. His ECG and chest radiograph were also within normal limits. It was thought that the patient was likely to have abnormalities of the local blood circulation which could have probably resulted in hypoglycaemia manifesting as repeated episodes of right sided hemi paresis. Therefore, a left carotid angiogram was performed. It revealed (See [Figure - 1] and [Figure:2]) widespread atheroselerotic changes in both the internal and external carotid vessels. The posterior communicating artery region was the most severely affected.

  ::   Discussion Top

The clinical manifestations of hypoglycaemia result either directly as a consequence of tissue glucose deficiency or indirectly as effects of hormones released in response to the low glucose[2]. These symptoms whose biochemical basis is still not completely understood & are highly varied, including headache visual changes, mental status changes, focal neurological signs and ultimately coma and death. In contrast to acute hypoglycaemia, gradual fall in the blood glucose levels is especially likely to occur at night and shows up as slow, confused thinking, passivity, drowsiness, impaired initiative sometimes with a transiently impaired memory and judgement [7]. Prompt restoration of glucose to normal levels usually leads to complete recovery but prolonged hypoglycaemia can cause irreversible neurological damage similar to that caused by hypoxia[4].
In a recent review of all known cases of drug-induced hypoglycaemia, sulfonylureas were responsible in 504 patients out of a total of 778 cases[5]. However, it is estimated that only 5% of all patients on sulfonylureas have a hypoglycaemic reaction[5]. Acute or chronic malnutrition almost always accompanies hypoglycaemia. Other predisposing factors include increasing age, hepatic or renal insufficiency or adrenocortical insufficiency. In addition, action of sulfonylureas may be potentiated by alcohol, sulfonamides and salicylates[4]. Hypoglycaemia is assumed to result both from excessive release of insulin and because of direct inhibition of hepatic glucose output.
Functioning of the brain requires a constant supply of glucose and oxygen from the bloodstream. Under normal (and hypoglycaemic) conditions it can only partially utilize fatty acids or ketone bodies for its energy requirements. Therefore hypoglycaemia can affect all the cerebral neurons resulting in a generalized neuronal dysfunction. However, localized abnormalities in the cerebral circulation may lead to focal manifestations[1]. Both these features were documented in our patient, in whom hypoglycaemia manifested as repeated episodes of right sides hemi paresis, which completely cleared following intravenous glucose administration. In the light of this observation, the history of repeated right-sided weakness could also be probably related to a hypoglycaemic reaction rather than TlAs, since it would invariably clear after a cup of tea. Moreover, repeated episodes of TIAs are known to leave behind some signs of residual neurological deficits in the form of increased tone or brisk reflexes, none of which were noticed in our patient.
The documentation of the extensive atheroselerotic changes, especially in the region of Posterior Communicating and the anterior choroidal artery is significant, in the context of blood supply to the internal capsule. It explains our patient's repeated stereotyped presentation with hemi paresis, hernia aesthesia and homonymous hemia-nopia suggestive of a lesion in the internal capsule. On the other hand, the extensive atherosclerotic changes themselves would have been an adequate explanation for the development of multiple TIAs based on a cerebral hypo perfusion mechanism, but for the bio chemically documented evidence of hypoglycaemia.

  ::   Acknowledgments Top

We thank the Dean, Seth GS Medical College and King Edward Memorial Hospital, Parel, Bombay, for permission to publish this case report.

  ::   References Top

1. Adams RD, Victor M. Cerebrovascular diseases. In: “Principles of Neurology.” IIIrd Edition. New York: McGraw-Hill Book Company; 1985, pp 569-640  Back to cited text no. 1    
2.Ensinck JW, Williams RH. Disorders causing hypoglycaemia. In: “Textbook of Endocrinology. RH Williams, editor. 6th Edition. Philadelphia: WB Saunders Co; 1981, pp 844-875.  Back to cited text no. 2    
3.Ferrendelli JA. Hypoglycaemia and the central nervous system. In: 'Brain Work. The Coupling of Function, Metabolism and Blood Flow in Brain," Proceedings of the Alfred Benzon Symposium VIII. DH Ingrar, NA Lassen, editors. Copenhagen, Munksgaard; 1975, pp 298-311.  Back to cited text no. 3    
4.Holmes CS, Hayford JT, Gonzalez JL, Weydert JA. A survey of cognitive functioning at different glucose levels in diabetic persons. Diabetic Care 1983; 6:100-109.  Back to cited text no. 4    
5.Seltzer HS. Severe drug-induced hypoglycaemia: A review. Comper Therapy 1979; 5:21-57.  Back to cited text no. 5    
6.Sherwin RS, Felig P. Hypoglycaemia. In: "Endocrinology and Metabolism. P Felig, JD Baxier, AE Broadus, L A Frohman, editors. 2nd Edition, New York: McGraw-Hill Book Co.; 1987, pp 1179-1202.  Back to cited text no. 6    
7.Smith RJ. Hypoglycaemia. In: “Joshlin's Diabetes Mellitus.” A Marble, LP Krall, RF Bradley, AR Christlieb, JS Soeldner, editors. 12th Edition, Philadelphia: Lea and Febiger; 1985, pp 867-881.   Back to cited text no. 7    

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