Annals of Indian Academy of Neurology
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Year : 2007  |  Volume : 10  |  Issue : 4  |  Page : 270-271

Kleine-Levin syndrome in tubercular meningitis

1 Department of Neurology, B. R. D. Medical College, Gorakhpur, Uttar Pradesh - 273 013, India
2 Department of Medicine, B. R. D. Medical College, Gorakhpur, Uttar Pradesh - 273 013, India
3 Department of Pharmacology, B. R. D. Medical College, Gorakhpur, Uttar Pradesh - 273 013, India

Correspondence Address:
Jamal Haider
Department of Pharmacology, B. R. D. Medical College, Gorakhpur, Uttar Pradesh - 273 013
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-2327.37823

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Kleine Levin syndrome is a rare syndrome that involves hypersomnolence, megaphagia and psychiatric disturbances of unknown etiology and pathogenesis. A 16-year-old male with tuberculous meningitis developed hypersomnia and megaphagia with cranial magnetic resonance imaging (MRI) showing increased T2 hyperintensity in the cerebral peduncles and left occipital cortex. Antitubercular therapy led to the disappearance of clinical symptoms and MRI changes.

Keywords: Kleine Levin syndrome, tubercular meningitis

How to cite this article:
Thacker AK, Aeron A, Haider J, Rao K M. Kleine-Levin syndrome in tubercular meningitis. Ann Indian Acad Neurol 2007;10:270-1

How to cite this URL:
Thacker AK, Aeron A, Haider J, Rao K M. Kleine-Levin syndrome in tubercular meningitis. Ann Indian Acad Neurol [serial online] 2007 [cited 2021 Aug 1];10:270-1. Available from:

   Introduction Top

A syndrome of morbid hunger and periodic somnolence was first reported in 1932, and it was named as  Kleine-Levin syndrome More Details (KLS) 10 years later. The integral features of KLS are male preponderance, onset in adolescence, spontaneous disappearance of the syndrome along with megaphagia and pathological sleep. The syndrome has unknown pathogenesis with no established cause. The autopsy reports of occasional patients suggested a viral etiology. We document a case of KLS in association with tuberculous meningitis (TBM). This association has not been illustrated thus far.

   Case Report Top

A 16-year-old male presented with fever, headache and vomiting for 20 days. Fever was moderate and was associated with generalized headache of progressive severity. He also noticed blurring of vision, particularly in the left eye. During the course of illness, his family noted that gradually his appetite increased and he used to sleep more often. His craving for food followed a spell of sleep and his intake became voracious. This continued for more than 2 weeks and this forced his family to consult physicians. On arrival, it was noted that he slept for 2-3 hours and woke up with heavy intake of food. Such cycles started from 6 a.m. in morning and used to recur 5-6 times in the day. His urge for food was so severe that on waking up if he was not provided with food immediately, he used to rush to food items lying with the nearby patients in the ward. His usual daily intake included 50-60 chapatis , 5-6 L of milk, 2 large loaves of bread, 2 dozen bananas and 1 kg of grapes apart from dal , vegetables, eggs and any thing that he could lay his hands on. In fact, his father claimed that this heavy food intake for 2-3 weeks reduced him to a state of penury. He had no history of hyper-sexuality, seizures, weight loss or any history of drug intake.

On examination, he presented as an overweight young boy with fever of 100F.

Most of the time, he was found to be sleeping or consuming food. On arousal, he was responsive and he seemed content on completing his meals. His pulse and blood pressure were normal. CNS examination revealed an alert boy with secondary optic atrophy on left side. The remaining cranial nerves were normal. He had no motor or sensory deficit. There was mild hyperreflexia on the right with extensor plantar response on the same side. Meningeal signs were present as neck stiffness and Kernig's sign. Cardiovascular, respiratory and abdominal examinations were not contributory.

On investigation, his hemogram showed normal Hb, total and differential counts. His ESR was 51 mm in the first hour. Blood biochemistry for sugar revealed normal fasting and postprandial blood sugar, serum creatinine, liver enzymes and electrolytes. The cerebrospinal fluid was straw colored with fibrin clot and raised protein (71.0 mg/dl) and normal sugar (53 mg/dl). Cerebrospinal fluid (CSF) cell count was 35 cells/cubic mm, mainly lymphocytes (95%). CSF PCR for M. tuberculosis was positive. CSF hypocretin-1 was not measured. EEG revealed diffuse theta and delta slowing, more markedly on the left side. His MRI of the head revealed a focal area of increased signals on flair0 sequences around the left occipital cortex alongwith well defined bilateral T 2 hyper intensity in the cerebral peduncles [Figure - 1],[Figure - 2]. Repeat MRl 6 months later showed the complete disappearance of these lesions.

The patient was given antitubercular therapy with 4 drugs (RHEZ) and prednisolone. His appetite slowly returned to normal, and sleep pattern improved in the next 2 weeks. He was amnestic about his episodes of hyperphagia and hypersomnolence, but had a sense of guilt about missing his school. Following the completion of his ATT, he developed occasional agitation followed by aggression, insomnia and psychosis. He has been prescribed olanzapine (10 mg HS).

   Discussion Top

The patient fulfils all the four attributes of KLS and has a definitive diagnosis of tuberculous meningitis, although the cause and effect of TBM and KLS are difficult to establish. The etiopathogenesis of KLS in unknown and a purely psychiatric basis or hypothalamic involvement has been debated. [1],[2],[3] The only autopsy study showed the lesions in KLS to be present in thalamus, as inflammatory cells infiltration, perivascular cuffing with focal gliosis. These changes were most marked in the intralaminar nuclei and the medial nuclei. [1] Lesions of the medial thalamic nuclei are associated with vegetative and psychic disturbances in memory and temporal orientation. [4]

Hyperphagia, the other component of KLS seems to defy explanation on the basis of thalamic lesions. It has been assumed that periodic stimulation or functional ablation of some unidentified pathways integrating hunger with arousal in the posteromedial thalamus might be responsible for hyperphagia in KLS. [1] In fact, single photon emission computed tomography subtraction studies during symptomatic stage show bilateral hypoperfusion of thalami, hypothalamus, basal ganglia and medial and dorsolateral frontal regions, suggesting diencephalic lesions. [5]

Autopsy studies have suggested localized encephalitis as the cause of KLS. [6],[7] It seems that the end arteritis associated with tuberculous meningitis is responsible for features of KLS in our case, although angiographic confirmation is lacking. No consistent treatment is available for KLS, although lithium may be effective.

   References Top

1.Carpenter S, Yass R, Ochs R. A pathologic basis for Kleine-Levin syndrome. Arch Neurol 1982;39:25-8.  Back to cited text no. 1    
2.Critchley M. hypersomnia and megaphagia in adolescent males. Brain 1962;85:627-56.  Back to cited text no. 2    
3.Conklin CM, Tauntin IE. Kleine-Levin syndrome: A unique cause of fatigue in an athlete. Br J Sports Med 2005;39:e7.  Back to cited text no. 3    
4.Martin JJ. Thalamic syndromes. In: Vinken PI, Bruyn GW, editors. Localization in clinical neurology, vol. 2 in Handbook of clinical neurology. North Holland Publishing Co: Amsterdam; 1969.p. 469-96.  Back to cited text no. 4    
5.Huang Y, Kao PF, Guilleminan OL. Kleine Levin Syndrome and the thalamus. Program and abstracts of the 57 th annual meeting of American, Academy of Neurology. Miami Beach, Florida Presentation; April 9-16, 2005. p. 504.  Back to cited text no. 5    
6.Schaltenbrand G. Thalamus and Schalaf. Allg Z Psychiatr 1949;125:48-62.  Back to cited text no. 6    
7.Facon E, Steriade M, Wertheim N. Prolonged hypersomnia caused by bilateral lesions of the medial activator system: Thrombotic syndrome of the bifurcation of the basilar trunk. Rev Neurol (Paris) 1958;98:117-33.  Back to cited text no. 7    


  [Figure - 1], [Figure - 2]


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