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Biomedical subjects

G Pierangeli

Publications and source records attributed to G Pierangeli.

At least 19 recordsLinked to original sources
PubMed2006

Sleep--wake and body core temperature rhythms in multiple sclerosis with fatigue.

OBJECTIVE: To study sleep-wake and body core temperature (BCT) circadian rhythms in patients with multiple sclerosis (MS)-associated with chronic fatigue. METHODS: Six relapsing-remitting MS patients with chronic fatigue underwent 48 consecutive hours polysomnography (PSG) with BCT measurement, followed by a Multiple Sleep Latency Test (MSLT). All patients were relapse- and drug-free. Mood depression, brain and cervical cord enhanced MRI, dynamic spirometry and Fatigue Severity Scale (FSS) were assessed just before PSG. RESULTS: In all patients mood depression was absent and dynamic spirometry normal, but FSS confirmed fatigue. MRI showed non-enhancing lesions. Nocturnal sleep was characterized by normal architecture and mean sleep efficiency was only slightly reduced. Arousal index was normal and periodic limb movements during sleep (PLMS) were present in four patients, with an increased index (PLMS-I) in only two of them. Upon MSLT, mean sleep latency was normal in all patients with one sleep onset REM period in one patient. All patients displayed a normal BCT 24-h rhythm. Mesor, amplitude and acrophase of BCT rhythm did not show significant differences between MS and controls. CONCLUSIONS: We found substantially normal sleep-wake and BCT rhythmicity in six patients with MS and fatigue. Non-restorative sleep and abnormal BCT regulation were unlikely mechanisms of chronic fatigue in our MS patients. SIGNIFICANCE: Subjective fatigue and abnormal sleep and BCT can be independent manifestation in MS patients. The findings support the notion that objective measures of fatigue comparable to the MSLT for sleepiness do not exist.

Adult↗
PubMed2006

Study of hypothalamic metabolism in cluster headache by proton MR spectroscopy.

The authors used 1H-MRS to investigate hypothalamic metabolism in 26 patients with cluster headache (CH) and 12 healthy subjects. Hypothalamic N-acetylaspartate/creatine was reduced in patients with CH vs controls (p < 0.01). Dividing the patients into episodic CH outside- and in-cluster periods and chronic CH, the hypothalamic N-acetylaspartate/creatine in all three subgroups of patients was reduced. The reduction of the neuronal marker N-acetylaspartate is consistent with hypothalamic neuronal dysfunction in patients with CH.

Acute Disease↗
PubMed2006

Which therapy for which patient?

Prophylactic treatment is mainly intended to reduce the frequency of migraine attacks, enhance response to acute medications, improve patient function and reduce disability. Sufficient evidence and consensus exist to recommend propranolol, timolol, amitriptyline, pizotifen, divalproex, sodium valproate and topiramate as first line agents for migraine prevention. These drugs can halve the frequency of attacks in 50% of patients. The anticipated benefit must be weighed against the adverse effects associated with each agent in determining the optimal preventive regimen for individual patients considering any comorbid conditions that are often present. The decision to treat and the choice of prophylactic drug must be taken with the patient. It is important to balance expectations and therapeutic realities for each particular drug. Recent data on the effect of prophylactic treatment on trigeminovascular activation and on cortical spreading depression emphasise the importance of developing research on migraine-preventive drugs.

Adrenergic beta-Antagonists↗
PubMed2006

Chronic daily headache: risk factors and pathogenetic considerations.

Chronic daily headache (CDH) is a major clinical concern, although it is still plagued by difficulties with classification and definitions. CDH usually evolves from an episodic headache, mainly migraine. Drug overuse and other somatic or psychological traits are considered risk factors for CDH. The neurobiology underlying this clinical evolution is incompletely understood. There is evidence of a progressive dysfunction of central pain systems in some individuals probably genetically predisposed.

Chronic Disease↗
PubMed2006

A genetic association study of dopamine metabolism-related genes and chronic headache with drug abuse.

To assess the role of dopamine metabolism-related genes in the genetic liability to chronic headache with drug abuse (DA). We performed a genetic association study using four functional polymorphisms of the dopamine receptor 4 (DRD4), dopamine transporter (DAT), mono-amino-oxidase A (MAOA) and cathecol-O-methyl-transferase (COMT) genes in 103 patients with chronic daily headache associated with DA (CDHDA). Control samples were 117 individuals without headache or DA (controls) and 101 patients with episodic migraine without aura and without DA (MO). No differences were found at the COMT and MAOA genes among the three groups investigated. Allele 4 of DRD4 was significantly overrepresented in patients with MO compared with both controls and CDHDA. Allele 10 of the DAT gene was significantly underrepresented in patients with CDHDA when compared with the MO group. Genetic variability at the DRD4 gene is involved in the predisposition to episodic MO but not to DA, while liability to CDHDA may involve genetic variability at the DAT gene in comparison with episodic MO.

Adult↗
PubMed2005

Pharmacogenetics of headache treatment.

Headaches and migraines are widely prevalent diseases causing relevant disability and worsened quality of life. Several pharmacological options are available for headache therapy, mostly however without firm rationales and all having high rates of non-responders and often serious side effects. Variability of therapeutic effect and adverse events depend at least in part upon genetic variability, but the genetic factors involved are mostly unknown. Pharmacogenetics, i. e., the application of the knowledge of genomic diversity to the analysis of the phenotypic traits involved in therapeutic response and adverse events, is still in its infancy, but represents a promising approach to therapy in migraine. The extant evidence is summarised here, with special attention to pain therapy and the pharmacogenetics of the serotonergic and the dopaminergic systems.

Dopamine↗
PubMed2005

Generalised anhidrosis: different lesion sites demonstrated by microneurography and skin biopsy.

Generalised anhidrosis (GA) shows a uniform clinical picture whether the pathogenesis involves intrinsic abnormalities of sweat glands or postganglionic sympathetic cholinergic nerve dysfunction. We describe two patients who presented intolerance to heat and anhidrosis. In the first patient, symptoms started at 33 years of age, and were associated with absent tendon reflexes and a mydriatic right pupil unreactive to light. The other patient had been unable to sweat since birth. GA was diagnosed on the basis of clinical findings and thermoregulatory tests. Microneurography and morphological analysis of the skin and its innervation disclosed a different lesion site underlying GA in the two patients, and distinguished between a postganglionic autonomic nerve fibre lesion and sweat gland dysfunction.

Adult↗
PubMed2004

The role of cardiac diseases in the comorbidity between migraine and stroke.

Several case-control and cohort studies have suggested an association between migraine and stroke. A significantly higher risk for stroke was found in women under the age of 45 years and for the subgroup with migraine with aura, the posterior circulation being significantly more frequently involved. The link between cardiac diseases and the comorbidity migraine-stroke has been evaluated considering both possible relationships: a higher prevalence of a vascular disease involving both heart and brain in migraineurs, or a cardiac disorder, more prevalent in migraineurs, with a possible aetiological role in migraine attacks.

Aortic Aneurysm↗
PubMed2004

Headache and hypertension.

Headache is generally regarded as a symptom of high blood pressure in spite of conflicting opinions on the association of headache and arterial hypertension. Most studies have shown that mild chronic hypertension and headache are not associated and this demonstration needs to be implemented in clinical practice. Whether moderate hypertension predisposes to headache remains controversial, but there is little evidence that it does. Headaches caused by significant disturbances in arterial pressure are included in the section "Headache attributed to a disorders of homeostasis" (code 10.3) of the 2nd edition of the International Classification of Headache disorders.

Adrenal Gland Neoplasms↗
PubMed2003

A genetic association study of migraine with dopamine receptor 4, dopamine transporter and dopamine-beta-hydroxylase genes.

We assessed the role of some dopamine metabolism genes in the genetic susceptibility to migraine. We performed an association study using three functional polymorphisms: a 48-base-pair (bp) tandem repeat in the D4 dopamine receptor gene ( DRD4), a 40-bp tandem repeat in the dopamine transporter gene ( DAT) and a dinucleotide repeat in the dopamine beta-hydroxylase ( DBH) gene. Allelic and genotypic frequencies for each polymorphism were assayed in two migraine populations (93 individuals with migraine with aura (MA) and 101 with migraine without aura (MO)) and were compared with those in a control group (117 individuals). No significant differences were found between control and migraine groups for DAT and DBH polymorphisms. Instead, the distribution of alleles for the DRD4 gene in the MO group was significantly different from those in both MA and control groups, with the shortest and longest alleles being less frequent in MO. Our data indicate that MO, but not MA, shows significant genetic association with DRD4.

Adolescent↗
PubMed2003

The genetics of chronic headaches.

Patients with chronic daily headaches (CDH) bear similarities to drug or substance abuse patients, for whom genetic liability loci have been implicated. We reviewed papers dealing with the metabolic and the genetic aspects of CDH. The relative risk for CDH in first-degree relatives is 2.1- to 3.9-fold increased compared to the general population. Genetic variation at the dopamine receptor 2 has been associated with co-morbidity of migraine with aura with major depression and anxiety, and allele D of the angiotensin converting enzyme increases the frequency of migraine without aura attacks. In CDH, analgesic abuse was significantly associated with specific functional polymorphisms at the DRD 4 and at the dopamine transporter (DAT) genes, findings implicating dopamine-related genes in CDH with drug abuse. CDH carries a substantial genetic predisposition. Molecular genetic studies are, however, still few and preliminary.

Biological Factors↗
PubMed2003

Chronic pain-autonomic interactions.

The nociceptive and the autonomic nervous systems interact at the levels of the periphery, spinal cord, brainstem, and forebrain. Spinal and visceral afferents provide converging information to spinothalamic neurons in the dorsal horn and to neurons of the nucleus tractus solitarius and parabrachial nuclei. These structures project to areas involved in reflex, homeostatic and behavioral control of autonomic outflow and nociception. Clinical and experimental observations on migraine suggest that a general hyperexcitability could develop along nociceptive trigeminal neurons allowing the activation of descending pathways that facilitate pain processing or the suppression of pathways that slow down pain transmission. Slowly progressive dysfunction of central pain systems secondary to the repetition of attacks of the originating headache has been implicated in transforming the process from an episodic to a chronic condition. This concept of an irritable focus in the central nervous system is currently known as "central sensitization" and is a characteristic feature of visceral pain. Considering primary headache as the result of the interactions between the nociceptive and autonomic systems (visceral pain) can help us to understand the complex pathophysiology of these disorders and to explore new treatments.

Animals↗
PubMed2002

Paroxysmal episodic central thermoregulatory failure.

A 51-year-old man presenting with paroxysmal attacks of unilateral sweating for 1 year was studied. Clinical and laboratory findings made the diagnosis of Shapiro or Harlequin syndrome unlikely. The onset of the sweating "crisis" was immediately followed by a progressive decrease in rectal and skin temperature, lasting for about 2 hours. This indicated that hypothermia was related to an abnormal downward shift of the thermoregulatory set point and a delayed effect of mechanisms blocking heat dissipation.

Autonomic Nervous System↗
PubMed2002

Familial hemiplegic migraine: clinical features and probable linkage to chromosome 1 in an Italian family.

We describe an Italian family with familial hemiplegic migraine (FHM), subtle cerebellar signs and probable linkage to chromosome 1. FHM is genetically heterogeneous; in about 50% of families it is caused by mutations within the CACNA1A gene on chromosome 19. Linkage to 1q31 and 1g21-23 has also been established. Other families do not link either to chromosome 19 or 1. Chromosome 19-linked FHM may display nystagmus and cerebellar ataxia. Affected family members were neurologically examined; linkage analysis was performed with markers for chromosomes 19p13, 1q21-23, and 1q32. Five family members had hemiplegic migraine, and 3 displayed additional cerebellar signs (scanning speech and nystagmus). In 1 patient, episodes of hemiplegic migraine triggered by mild head trauma. Epilepsy and mental retardation were also found in 1 affected relative each. Lod scores for linkage to 19p13 were negative, while the maximum two-point lod score was 1.81 to 1q21-23. This family with FHM and associated subtle cerebellar signs, epilepsy and mental retardation showed probable linkage to 1q21-23.

Adult↗
PubMed2002

Bilateral paramedian thalamic syndrome: abnormal circadian wake-sleep and autonomic functions.

OBJECTIVES: To describe wake-sleep and body core temperature (t degrees ) rhythm abnormalities in two patients with bilateral paramedian thalamic calcifications. METHODS: Patients underwent (18F)FDG PET scans and 24 hour polygraphic recordings of wake-sleep and t degrees. RESULTS: PET showed bilateral thalamic hypometabolism in both patients with additional basal ganglia or mesiolateral frontal and cingular hypometabolism. Wake-sleep studies showed abnormal sleep organisation and in the case with frontal and limbic PET hypometabolism, pre-sleep behaviour associated with "subwakefulness" EEG activities, lack of EEG spindles and K complexes, and features of status dissociatus. The t degrees rhythms showed increased mesor in both (37.4 degrees C and 37.75 degrees C) and inverted rhythm in one patient. CONCLUSIONS: Paramedian thalamic structures and interconnected, especially frontal and cingular, areas play a part in the organisation of the wake-sleep cycle and attendant autonomic functions.

Autonomic Nervous System Diseases↗
PubMed2001

Deficient energy metabolism is associated with low free magnesium in the brains of patients with migraine and cluster headache.

We used phosphorus magnetic resonance spectroscopy to assess in vivo the brain cytosolic free magnesium concentration and the free energy released by the reaction of adenosine triphosphate (ATP) hydrolysis (DeltaG(ATPhyd)), the latter being an index of the cell's bioenergetics condition. We studied 78 patients with migraine in attack-free periods (7 with migraine stroke, 13 with migraine with prolonged aura, 37 with migraine with typical aura or basilar migraine, and 21 with migraine without aura), and 13 patients with cluster headache. In the occipital lobes of all subgroups of migraine and in cluster headache patients cytosolic free [Mg(2+)] as well as the free energy released by the reaction of ATP hydrolysis were significantly reduced. Among migraine patients, the level of free energy released by the reaction of ATP hydrolysis and the cytosolic free [Mg(2+)] showed a trend in keeping with the severity of clinical phenotype, both showing the lowest values in patients with migraine stroke and the highest in patients with migraine without aura. These results support our current hypothesis that the reduction in free [Mg(2+)] in tissues with mitochondrial dysfunction is secondary to the bioenergetics deficit, and are against a primary role of low brain cytosolic free [Mg(2+)] in causing the bioenergetics deficit in headache.

Adenosine Triphosphate↗