Post-traumatic headache: facts and doubts.

The International Classification of Headache Disorders does not separate the moderate from severe/very severe traumatic brain injury (TBI), since they are all defined by Glasgow coma scale (GCS) < 13. The distinction between the severe and very severe TBI (GCS < 8) should be made upon coma duration that in the latter may be longer than 15 days up to months in the case of vegetative state. Post-traumatic amnesia duration may double the coma duration itself. Therefore, the 3-month parameter proposed to define the occurrence or resolution of post-traumatic headache (PTH) appears inadequate. Following TBI, neuropathic pain, central pain, thalamic pain, combined pain are all possible and they call for proper pharmacological approaches. One more reason for having difficulties in obtaining information about headache in the early phase after regaining consciousness is the presence of concomitant medications that may affect pain perception. Post-traumatic stress disorder (PTSD) develops days or weeks after stress and tends to improve or disappear within 3 months after exposure; interestingly, this spontaneous timing resembles that of PTH. In our experience the number of TBI patients with PTH at 1-year follow-up is lower in those with longer coma duration and more severe TBI. Cognitive functioning evaluated after at least 12 months from TBI, showed mild or no impairment in these patients with severe TBI and PTH, whereas they have psychopathological changes, namely anxiety and depression. The majority of patients with PTH after severe/very severe TBI had skull fractures or dural lacerations and paroxystic EEG abnormalities. The combination of psychological changes (depression and anxiety) and organic features (skull fractures, dural lacerations, epileptic EEG abnormalities) in PTH may be inversely correlated with the severity of TBI, with prevalence of psychological disturbances in mild TBI and of organic lesions in severe TBI. On the other hand, only in severe TBI patients with good cognitive recovery the influence of the psychopathological disorders may play a role. In fact, the affective pain perception is probably related to the integrity of cognitive functions as in mild TBI and in severe TBI with good cognitive outcome.

The pathophysiology of migraine: year 2005.

Migraine is a complex patholophysiology in which both central and peripheral components of the trigeminal pain pathway probably play a significant role, both in the symptoms and signs of the attack and in the mechanisms of action of antimigraine compounds, such as triptans, which constitute the most important therapy for aborting migraine pain and possess several mechanisms on 5-HT receptor-mediated actions. The experimental neurogenic inflammation model represents a simple procedure to obtain preliminary information on well characterized receptortargeted drugs. The apparent paradox observed with certain drugs that are shown to be effective in this model but not in clinical trials offers the opportunity to better manipulate structure-activity to obtain the best pharmacological profile using an array of experimental models. The observation that nitric oxide donors induce migraine-like pain in migraineours and that nitric oxide plays a pivotal role in the control of several functions in the central nervous system, has prompted the use of such molecules for better understanding the pathophysiology of migraine attacks. A link between central and peripheral components of the trigeminal pain pathway is provided by the observation that cortical spreading depression in the rat activates trigeminovascular afferents and induces a series of cortical meningeal and brainstem events consistent with the development of headache. Studies in humans support the hypothesis that cortical spreading depression underlies migraine.aura. Therefore, tt is possible that visual, motor or sensory aura might be responsible for the generation of the pain through the above mechanisms.

Migraine disease: evolution and progression.

Migraine is a complex pathology and it should be regarded as a disease evolving during the lifetime along with other comorbid conditions. Migraine susceptibility may be unmasked by exogenous substances and the occurrence of migraine attacks may change following drugs given for therapeutical purposes. The evolution of migraine should be followed up because childhood migrainous manifestations may vary over the years and an earlier diagnosis may not apply later on.

Late motor recovery is influenced by muscle tone changes after stroke.

OBJECTIVES: To evaluate the time course of motor recovery in a poststroke period ranging from 2 to 6 months and its correlation with both the severity of motor deficit and the muscle tone disturbances (flaccidity or spasticity) of the affected limbs. DESIGN: Prospective cohort study. SETTING: A comprehensive rehabilitation hospital. PARTICIPANTS: Forty consecutive stroke patients (21 men, 19 women) with first ischemic stroke who met the inclusion criteria. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: Change in motor deficit as evaluated by the Adams Hemispheric Stroke Scale. RESULTS: Stepwise regression analysis indicated that the most significant factors influencing motor recovery were the time elapsed since stroke and muscle tone. CONCLUSIONS: Rehabilitation of stroke patients is more effective in the first months after the event rather than later, considering the significant correlation observed between motor recovery and time elapsed since stroke. Flaccid patients appear to need 3 months or more before reaching the final plateau, because motor recovery occurs later and/or proceeds more slowly, whereas outcomes for spastic patients with spasticity appears to occur in the first months after stroke.

Prodromes and the early phase of the migraine attack: therapeutic relevance.

A migraine attack is a multiphasic event. In some patients the initial phase of the attack is characterized by the presence of "prodromes" or "premonitory symptoms" which are not recognized by the patient as part of the attack. Premonitory symptoms are defined as "symptoms preceding and forewarning of a migraine attack by 2-48 hours, occurring before the aura in migraine with aura and before the onset of pain in migraine without aura". Migraine premonitory symptoms should be differentiated from aura and symptoms of premenstrual syndrome. This differentiation, which is crucial to correct diagnosis, is based on two principal aspects, namely, the timing of these premonitory symptoms prior to the headache pain and their clinical characteristics. The neurotransmitters dopamine and serotonin are possibly involved in the development of premonitory symptoms, as demonstrated by experimental models and by the efficacy of migraine aborting and preventive treatments. Accurate recording of premonitory symptoms may contribute to efforts to design the best therapeutic approach in migraine patients.

Prodromes and predictors of migraine attack.

Premonitory symptoms of migraine include a wide and heterogeneous collection of cognitive, psychic and physical changes preceding and forewarning of an attack by a few hours to 2-3 days. To date, premonitory symptoms have received little attention in the literature, being treated more as a curiosity than as a primary feature of migraine. This paper provides an extensive critical review of this neglected area of migraine research in the light of the recent advances in our understanding of the pathogenetic mechanisms of migraine. Epidemiological and clinical studies that have investigated the premonitory symptoms of migraine lack scientific rigour, producing conflicting results, whilst genetic and pathophysiological investigations are still in their very early stages. There is evidence supporting the idea that premonitory symptoms could be used as a phenotypical marker to identify subgroups of migraineurs which could show correlations with specific clinical expressions of the disease, genotypes, or responses to treatments. Future studies are needed to clarify the clinical, pathophysiological and therapeutic significance of premonitory symptoms.

Subcutaneous sumatriptan induces changes in frequency pattern in cluster headache patients.

OBJECTIVES: To document the relationship between the use of subcutaneous (SQ) sumatriptan (sum) and a change in frequency pattern of cluster headache (CH) in six patients. To discuss the clinical and pathophysiological implications of this observation in the context of available literature. BACKGROUND: Treatment with SQ sum may cause an increase in attack frequency of CH but data from literature are scant and controversial. METHODS: Six CH sum-naïve patients (three episodic and three chronic according to the International Headache Society (IHS) criteria) are described. RESULTS: All six patients had very fast relief from pain and accompanying symptoms from the drug but they developed an increase in attack frequency soon after using SQ sum. In all patients, the CH returned to its usual frequency within a few days after SQ sum was withdrawn or replaced with other drugs. Five patients were not taking any prophylactic treatment and SQ sum was the only drug prescribed to treat their headache. CONCLUSIONS: Physicians should recognize the possibility that treatment of CH with SQ sum may be associated with an increased frequency of headache attacks.

Chiari-associated exertional, cough, and sneeze headache responsive to medical therapy.

Benign exertional headache is coded as a separate entity within the International Headache Society's classification system, but the pathophysiological mechanisms underlying this clinical headache subtype are unknown and possibly are similar to those generating migraine. Coexistence of migraine and benign exertional headache in the same patient is not unusual, and antimigraine pharmacologic treatments are often effective in both headache types. Regardless, optimal management mandates that the clinician exclude any intracranial or systemic disease that could mimic "primary" exertional headache. The same holds for primary headaches induced by coughing or sneezing; congenital malformations or neoplasms, particularly within the posterior fossa, are not rare in these patients. The neurologic examination may not be sufficiently sensitive to detect the offending lesion. We describe a patient with migraine without aura and exertional secondary headache due to Chiari malformation type I whose headaches responded to treatment with propranolol and indomethacin.