Vinod Kumar Gupta

Recurrent syncope, hypotension, asthma, and migraine with aura: role of metoclopramide.

Migraine associated with asthma or symptomatic orthostatic hypotension is a particularly difficult subgroup to manage. Metoclopramide is a useful pharmacological agent for orthostatic hypotension. I present the case report of a migraine patient with asthma and recurrent hypotensive syncope. Metoclopramide relieved recurrent syncope as well as migraine attacks in this patient. Metoclopramide has a striking influence on arginine vasopressin (AVP) secretion. AVP promotes antinociception and influences vasomotor and behavior control, which actions possibly keep migraine in remission. Further studies are necessary to confirm the migraine prophylactic value of metoclopramide.

Ocular Compression Maneuver Aborts Benign Cough-Induced Headache

Benign cough‐induced headache is a short‐lasting cranial discomfort. The therapeutic role of lumbar puncture (LP) or indomethacin in benign patients with benign cough‐induced headache patients is debatable. Transient ocular compression (OC) raises intraocular pressure (IOP) and can limit the impact of cough‐induced choroidal venous congestion. A self‐applied maneuver that instantaneously aborts cough‐induced headache is described in two patients. The effect of this maneuver supports a recent hypothesis that cough‐induced headache may be due to ocular choroidal venous congestion and mechanical antidromic trigeminal nerve activation. The OC maneuver has several potential complications and its self‐application in benign cough‐induced headache should be regarded as an experimental procedure until more data regarding its efficacy and safety become available.

Cortical Spreading Depression Is Neuroprotective: The Challenge of Basic Sciences

Hall et al (Headache. 2004;44:204-208) recorded cortical activity during migraine visual aura using magnetoencephalography. These authors conclude that their results are consistent with the theory of cortical spreading depression (CSD). If CSD is the neuro-physiological equivalent—and basis—of the migraine aura, it cannot be the attack-initiating event because the migraine prodrome—that precedes both the headache as well as the aura—can last several hours or a few days.1 About 20 years ago, Pearce underscored that CSD is not the inaugural event at the level of the brain.2 The advent of sophisticated neuroimaging does not diminish the importance of such fundamental pathophysiological considerations. Any theoretical model must correspond with clinical reality, by which benchmark the theory of CSD has serious drawbacks.3,4 Pharmacological agents that do not cross the blood-brain barrier (BBB) instantaneously abort migraine aura.4 In cats, CSD is not associated with release of calcitonin gene-related peptide.5 Dihydroergotamine, acetylsalicylic acid, metoprolol, or valproate do not affect CSD in the cat.6 Spreading depression cannot be elicited in the brain stem of the adult rat, even after conditioning.7 The brain stem is the focus of several pathogenetic concepts for migraine. Premature philosophic commitment encourages scientists to ignore contradictory evidences. A Medline review reveals a number of studies that show the neuroprotective effect of CSD following brain injury or ischemia.8,9 CSD is a powerful yet largely benign stimulus that acutely is capable of providing long-lasting ischemic tolerance probably through ischemic preconditioning; prolonged increase in atrial natriuretic peptide after an acute episode of CSD possibly contributes to CSD-induced neuroprotection.10 The neuroprotective effect of CSD has been known since about two decades; needle puncture of the brain improves survival following forebrain ischemia in mice.11 There is little evidence to support the popular belief that CSD is an important brain pathophysiological mechanism. Insofar as migraine pathophysiology is concerned, the ability of atenolol—that does not cross BBB—to prevent migraine with or without aura heralds the demise of a popular neurological theoretical concept.12 The scientific imperative to explain occurrence of migraine aura must not dull our ability to think logically.

Triptans to Abort Neurological Symptoms of Prodrome of Migraine: Fact or Fiction?

The age of onset in cluster headache may vary. However, most of the patients experience the first attacks between 20 and 30 years of age.1 We have recently described two patients with a very late onset cluster headache.2 Here, we describe the case of a patient with—to our knowledge—the oldest age of onset of typical cluster headache. An 89-year-old woman presented to the neurological inpatient clinic because of severe headache attacks for 4 months. The attacks occurred about two or three times a day and lasted between 20 and 45 minutes. They were strongly right sided, accompanied by redness and tearing of the right eye. There was a nasal congestion on the right side. The patient was not aware of any trigger factors. She never had attacks like this before in her life, and there was no evidence for dementia. The family history was free of headache disorders. Another neurological hospital suspected trigeminal neuralgia and treated her with gabapentin. This and simple analgesics were without any effect. An MRI scan of the skull was unremarkable as was the neurological examination. The woman was very healthy for her age and did not show any mental disorders. She was treated with sumatriptan (3 mg subcutaneously) that stopped the attacks after about 10 to 15 minutes. A prophylactic treatment with verapamil was started and increased up to 240 mg per day. The diagnosis of cluster headache was made based on a total observation period of 10 days. After starting the prophylactic medication, the woman did not complain of any further attack. The oldest age of onset in cluster headache described in the previous literature was—to the best of our knowledge— 71 years3 and 83 years.2 Our case shows that the age of onset in cluster headache may be even higher. Therefore, it has to be considered in future epidemiologial and genetic studies that the age of onset in cluster headache may vary widely and that a clinically asymptomatic patient even in higher ages will not necessarily be free of cluster headache for all his life.

Migraine, epilepsy, and brain neuronal hyperexcitation.

Mateo et al report a patient with repeated episodes of migraine-associated seizures with reversible brain magnetic resonance imaging (MRI) abnormalities.1 A critical issue regarding the brain MRI findings observed in this case is whether the fleeting structural changes in the brain parenchyma are primarily or pathogenetically related to the headache. Whereas the headaches were strictly lateralized in all migraine attacks, the neurologic deficits did not correspond neuroanatomically; also brain MRI changes, although consistent with the neurologic symptoms of the episode, varied in their distribution during discrete attacks. It seems reasonable to conclude that MRI changes recorded in this patient and in other studies reflect secondary changes consequent to the physiological changes accompanying or consequent to the headache.2 Considering the possibility of triggering of seizures by aura of migraine, the absence of paroxysmal activity in the electroencephalogram (EEG) in this adult patient is a striking feature. Children and adolescents are particularly predisposed to such attacks.3 Incidence of abnormal interictal EEGs in migraine and tension-type headache patients is approximately equal; epileptiform activity, rather paradoxically, occurs more commonly in the latter.4 Moreover, as reviewed by Bazil, both migraine and seizures in such patients can be controlled by nimodipine, verapamil, or nifedipine.5 These calcium-channel antagonists do not cross the blood-brain barrier (BBB). Pathophysiologically, the ability of pharmacological agents that do not freely cross BBB to remit migraine and migraine-associated seizures cannot be overemphasized.6 The remission of migraine and migraine-associated seizures by calcium-channel antagonists (other than class IV flunarizine-like agents) seriously challenges the putative pathogenetic role of cortical spreading depression. Amitriptyline is effective for migraine prophylaxis. The epileptogenic potential of tricyclic antide pressants (TCA), however, is well established.7 Despite being used commonly for management of migraine, amitriptyline has not manifested an increased tendency for migraine patients to manifest epilepsy. In other words, migraine itself is not a risk factor for antidepressant-related seizures. Amitriptyline can be considered for the management of otherwise refractory migraine-associated seizures. It is surprising that in the absence of a specific contraindication, propranolol was not considered for the management of this patient. Vinod Kumar Gupta, MD Physician, Dubai Police Medical Services P.O. Box 12005, Dubai United Arab Emirates

Migraine and Sex Hormones: Epidemiological Data Stimulate Rethinking of Etiologic Role of Estrogen

I write to recount my personal case history to raise the possibility that obscure dental disease may be the cause of headache of unknown etiology and to question whether we have adequate investigative strategies to make such diagnoses. A few years ago, at about age 50, I began to experience right-sided headaches that significantly interfered with my quality of life, requiring regular use of analgesics. Assessments by an internist and otolaryngologist, including a CT head scan revealed no cause for the headaches. Concurrently, over the course of about 3 years, I also experienced a very few episodes of acute sharp lower right facial pain lasting a few seconds. Because of this, I sought attention from my dentist who repeatedly failed to find any evidence of a dental process. Approximately 3 years after the headaches began, I was referred for a consultation with an endodontist, whose evaluation included thermal testing. He found no significant pathology, but noted a very subtle shadowing at the apex of the root of a right maxillary tooth and offered to undertake a root canal of it if I became desperate. That night I experienced another brief episode of acute lower facial pain and I accordingly decided to proceed with this procedure. On undergoing the root canal, these headaches disappeared immediately and did not recur. After being headache-free for about a year, I began to experience left-sided headaches. Similar to those previously experienced, I was significantly impaired and required almost daily use of NSAIDs. Perhaps because of my previous experience, I wondered about a dental origin of the headaches. Sometimes I felt that the discomfort had a vague focus in the maxillary area and therefore I again sought dental assessments, which resulted in repeated negative investigations. I tried to identify a specific origin and came to suspect a particular tooth that had had a previous root canal. I was referred to another dentist for a second opinion, including thermal testing, which was negative, and for consideration of a revision of the root canal on the tooth of concern, which he declined to do. I was subsequently referred to the endodontist I had seen previously for an additional opinion. He was unable to find a dental cause for my symptoms, but because of his previous experience with me, offered to undertake a resection of the apex of the root of the suspect tooth. While waiting for this surgery, redness and swelling developed in the gum overlying the base of this tooth. It was now approximately 2 years into the course of this headache. While undergoing antibiotic therapy for “abscessing” of this tooth, my headache disappeared completely. At dental surgery the following week, no gross abnormality of the root apex was discerned and the headaches have not recurred to this point, now more than 6 months later. I have experienced a major problem of headaches that seem clearly to have been based on extremely subtle and difficult-to-diagnose dental disease, which makes me wonder if the diagnosis of a dental etiology in others with similar complaints goes unrecognized. This could occur because of an insensitivity to the possibility of such a connection and/or because of a lack of available tools to make such diagnoses. This may represent an area for further, potentially useful, enquiry.