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Year : 2006  |  Volume : 54  |  Issue : 2  |  Page : 205-206

Hypomania as an aura in migraine

1 Department of Psychiatry, Royal Cornhill Hospital, Aberdeen AB25 2ZH, United Kingdom
2 Department of Neurological Sciences, Apollo Hospitals, Hyderabad, India

Correspondence Address:
Soumitra Shankar Datta
Department of Psychiatry, Royal Cornhill Hospital, Aberdeen AB25 2ZH
United Kingdom
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Source of Support: None, Conflict of Interest: None

PMID: 16804272

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We report a 19-year-old man presenting to the department of Psychiatry for the evaluation of prominent behavioral symptoms associated with episodic headaches, with normal inter-episodic periods. A diagnosis of classic migraine with hypomanic aura was made. Other possible co-morbid or causative illnesses were excluded and preventive therapy with valproate was started due to the prominent affective symptoms as a part of the migranous aura. With this the frequency of headaches gradually decreased over the next four months. He was followed up for 2 years when he was found to be symptom-free. Recent research into the mechanisms of migraine has identified that the cortical hyperexcitability and an imbalance between neuronal inhibition and excitement mediated by gamma-aminobutyric acid and excitatory amino acids respectively may be the underlying mechanism. The high rate of affective disorders in patients with migraine, association of migraine with an aura comprising of mood symptoms and good response to treatment with mood-stabilisers might give newer insights into the pathophysiology of mood disorder as well.

Keywords: Migraine, hypomania, aura, sodium valproate

How to cite this article:
Datta SS, Kumar S. Hypomania as an aura in migraine. Neurol India 2006;54:205-6

How to cite this URL:
Datta SS, Kumar S. Hypomania as an aura in migraine. Neurol India [serial online] 2006 [cited 2023 Sep 24];54:205-6. Available from:

  Introduction Top

The diagnosis of migraine with aura, requires at least two migraine attacks with any three of the following four features: [a] One or more fully reversible aura symptoms (which could be visual, sensory or speech disturbance); [b] aura developing over a course of more than four minutes; or [c] aura lasting less than sixty minutes; and [d] headache following aura within sixty minutes.[1],[2] Here we present a case of migraine with aura with atypical features, who presented to the department of Psychiatry for the prominent behavioral symptoms as part of the aura of classic migraine. He would fall in the subtype of probable migraine with aura with atypical features (lasting longer than 60 minutes). His clinical course, response to treatment and condition at follow up is presented. Overlap of mood disorders and migraine might have implications for common biological etiology, life style factors, reactive factors to the transiently disabling and painful neurological illness and common treatment factors.

  Case Report Top

19-year-old young man presented to the outpatients' clinic of Psychiatry department with 4 years history of episodic headache. Each attack of headache in this patient was characterized by four stages: Stage I- Before getting an episode of headache he could anticipate it (aura). He would feel extremely happy. He would be hyperactive, demand money, express grandiosity. This stage would last for 15-20 minutes. Stage II- He would develop severe holo-cranial headache, throbbing in character associated with photophobia, phonophobia, photopsia and fortification figures. Visual symptoms lasted for 15-20 minutes. During this phase he would be extremely destructive, breaking up household articles, be abusive and assaultive towards family members. This phase would last approximately 4-5 hours. Stage III- Immediately after the headache he would sleep off for 1-2 hours. Stage IV- He would be extremely remorseful about his aggressive outburst. He would have full memory about the incidents and would be symptom-free till the next attack. Frequency of attacks in the beginning was approximately once in 1-4 weeks, which later gradually increased to once a day. He had no history of loss of consciousness, altered sensorium, automatisms, incontinence, tongue bite or injury due to any falls. He had full recall of events during attacks. He had no past history of depressive or manic episodes. He had no history suggestive of focal neurological deficits during episodes. The possibility of "secondary gain" was excluded. He had a family history suggestive of migraine in his maternal grandfather. He had never been treated for his illness. This patient had a normal birth and developmental history and had no history of childhood seizures or seizure equivalents.

General and systemic examination during episodes of headache and inter-morbid period were normal. A detailed neurological examination was normal. Investigations including blood counts and serum electrolytes, blood biochemistry were all within normal limits. A normal Magnetic Resonance imaging of brain and Electroencephalogram (EEG) ruled out any structural pathology and seizure activity. The differential diagnoses considered were temporal lobe epilepsy, migraine without aura associated to hypomanic symptomatology and migraine with aura. Since the patient had no other symptoms suggestive of seizure equivalents, had full recall of events that occurred in the entire episode, had other associated symptoms of migraine with aura and had a normal EEG tracing, the diagnosis of epilepsy was not considered. Hypomanic symptoms occurred in close association with migraine attacks, preceding the headache onset by 15-20 minutes and lasting during most of headache period. He had no hypomanic symptoms without the occurrence of headache.

Initially patient was started on Tab propranolol 40 mg once daily, with which he had symptomatic postural hypotension. Propranolol was then substituted with Tab sodium valproate (VPT), as this could help both the migraine and mood symptoms. VPT was started at a dose of 200 mg once daily and was gradually increased to 200 mg thrice daily according to the clinical response and serum level of valproate, optimizing between response and toxicity. On a daily dosage of 600mg of valproate, he maintained a serum level of 90µg/ml and had a good clinical response.

Follow up at 2 years: This patient had responded well to treatment. The frequency of headache reduced slowly over the four months following the initiation of therapy. He did not have a single episode of headache in the last one-year.

  Discussion Top

There is a strong cross-sectional relation between affective disorders and migraine.[3],[4] Mood change is also one of the commonest prodromal (premonitory) symptoms among migraineurs.[5] Psychiatric factors and migraine may interact in three general ways, etiologically, psychophysiologically or biobehaviorally and comorbidly (the two disorders coexist). The relation between the two disorders may be a result of chance or one disorder can cause another disorder (cause-effect relationship). Yet others have speculated that there might be shared environmental risks between migraine and mood disorders. Last, but not the least, there may be environmental or genetic risk factors that produce a brain state giving rise to both conditions, that is, there may be some common biology underlying both conditions.[6] Depression and anxiety are more common with migraine as co-morbid illnesses, as compared to mania or hypomania. In our current case, mood symptoms occurred as a part of the migraine headache more specifically the aura. It is worth mentioning that the patient had no mood symptoms inter-morbidly. In our opinion, mood symptoms occurring as part of migraine aura are rare. Another possibility to be considered in this patient would be premonitory symptoms. These symptoms that warn of an impending migraine headache have been recognized for many years. However, the ability of premonitory symptoms to accurately predict the migraine attack is doubtful.[7] In the above study, the most common premonitory symptoms noted were feeling tired and weary (72% of attacks with warning features), having difficulty concentrating (51%) and a stiff neck (50%). Subjects who functioned poorly in the premonitory phase were the most likely to correctly predict headache. Another study reported the occurrence of prodromal symptoms in about a third of migraine patients that lasted on an average of 7-9 hours.[8] The most common symptoms were tiredness, mood change and gastrointestinal symptoms. Although it is difficult to ascertain whether the hypomanic symptoms in our patient were prodromal symptoms or occurred as part of aura; the possibility of them being symptoms of aura is higher as all those episodes were followed by occurrence of migraine headache.

The patient had complete remission of symptoms after treatment with a potent mood stabiliser (VPT). Currently the role of VPT in migraine prophylaxis is well documented.[9],[10],[11],[12]

In conclusion, mood changes such as hypomanic features may occur as part of migranous aura and should be clinically recognized as such. Sodium valproate is effective in these cases and leads to remission of symptoms. This observation may imply common pathophysiologic mechanisms underlying migraine and mood disorders. However, it is emphasized that the association of hypomania and migraine and their improvement with VPT could be a co-incidence and this finding needs to be corroborated with more case reports.

  References Top

1.Headache Classification Committee of the International Headache Society. Int Class Headache Dis Cephal 2004;24:1-160.   Back to cited text no. 1    
2.Silberstein SD, Lipton RB. Overview of diagnosis and treatment of migraine. Neurology 1994;44:6-16.   Back to cited text no. 2  [PUBMED]  
3.Swartz KL, Pratt LA, Armenian HK, Lee LC, Eaton WW. Mental disorders and the incidence of migraine headaches in a community sample: results from the Baltimore Epidemiologic Catchment area follow-up study. Arch Gen Psychiatr 2000;57:945-50.   Back to cited text no. 3  [PUBMED]  [FULLTEXT]
4.Radat F, Swendsen J. Psychiatric comorbidity in migraine: a review. Cephalalgia 2005;25:165-78.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]
5.Kelman L. The premonitory symptoms (prodrome): a tertiary care study of 893 migraineurs. Headache 2004;44:865-72.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Sheftell FD, Atlas SJ. Migraine and psychiatric comorbidity: from theory and hypotheses to clinical application. Headache 2002;42:934-44.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Giffin NJ, Ruggiero L, Lipton RB, Silberstein SD, Tvedskov JF, Olesen J, et al . Premonitory symptoms in migraine: an electronic diary study. Neurology 2003;60:935-40.   Back to cited text no. 7    
8.Kelman R. The premonitory symptoms (prodrome):a tertiary care study of 893 migraineurs. Headache 2004;44:865-72.  Back to cited text no. 8    
9.Mathew NT. Antiepileptic drugs in migraine prevention. Headache 2001;4:S18-24.  Back to cited text no. 9  [PUBMED]  
10.Chronicle E, Mulleners W. Anticonvulsant drugs for migraine prophylaxis. Cochrane Database Syst Rev 2004;3:CD003226.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Fragoso YD. Low dose of sodium divalproate for the treatment of migraine. Med Gen Med 2003;12:32.  Back to cited text no. 11    
12.Kinze S, Clauss M, Reuter U, Wolf T, Dreier JP, Einhaupl KM, et al . Valproic acid is effective in migraine prophylaxis at low serum levels: a prospective open-label study. Headache 2001;41:774-8.  Back to cited text no. 12    

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