Tail-pinch-induced hyperphagia in weanling rats with dorsomedial hypothalamic lesions

Dorsomedial hypothalamic lesions (DMNL) were produced in 26-day-old and 44-day-old male rats. Sham-operated rats served as controls. Tail-pinching (TP) was performed for five minutes at a time over two periods: the first TP period of six sessions each from post-operative day 1 to day 17 and the second TP period of eight sessions from post-operative day 18 to day 35. Three equicloric diets, high-carbohydrate, high-fat, and high-protein, were presented ad libitum in pellet form during the TP sessions. Lab chow was available ad libitum in the home cages. Rats with DMNL at age 26 days did not show TP-induced hyperphagia and HCD preference compared to the controls until the second TP period. In rats lesioned at age 44 days, TP-induced hyperphagia and HCD-preference (compared with controls) became evident immediately after the operation. In the home cages (lab chow), DMNL rats showed a decline in food intake from the first to the second TP period, while the sham-operated controls showed an increase. TP-induced hyperphagia in the rat with DMNL does not appear to be caused by some arousal-related process as has been shown for the rat with lateral hypothalamic lesions. Lesions in the nigrostriatal system have been reported to attenuate TP-induced feeding, while the present study indicates that lesions in the DMN enhance it. This suggests that fibers in the central nervous system may be involved in facilitation or inhibition of TP-induced eating.     

Medial prefrontal cortex activity associated with symptom provocation in eating disorders

OBJECTIVE: The authors sought to identify neural correlates of eating disorders in order to contribute to the debate on the genesis and classification of eating disorders and provide endophenotypes for genetic research. METHOD: Twenty-six female patients with eating disorders (10 with bulimia nervosa, 16 with anorexia nervosa) and 19 healthy female comparison subjects matched for age and education were presented with food and aversive emotional images while brain activity was recorded with functional magnetic resonance imaging. RESULTS: Women with eating disorders identified the food stimuli as threatening and disgusting. In response to these stimuli, the women with eating disorders had greater activation in the left medial orbitofrontal and anterior cingulate cortices and less activation in the lateral prefrontal cortex, inferior parietal lobule, and cerebellum, relative to the comparison group. In addition, women with bulimia nervosa had less activation in the lateral and apical prefrontal cortex, relative to the comparison group. Between-group differences in response to nonspecific emotional stimuli were found in the occipital cortex, parietal cortex, and cerebellum. CONCLUSIONS: A medial prefrontal response to symptom-provoking stimuli was identified as a common feature of anorexia and bulimia nervosa. This finding supports a conceptualization of eating disorders as being transdiagnostic at the neural level. The abnormal prefrontal reaction is associated with symptom-related material, whereas the occipital and cerebellar differences are nonspecific. An abnormal propensity to activate medial prefrontal circuits in response to inappropriate stimuli is common to eating, obsessive-compulsive, and addictive disorders and may account for the compulsive features of behavior in these conditions.     

Medial preoptic and hypothalamic neuronal activity during sexual behavior of the male monkey

Neuronal activity changes in the medial preoptic area of the male monkey were related to the commencement of sexual behavior, penile erection and the refractory period following ejaculation.Increased neuronal activity in the dorsomedial hypothalamic nucleus was found to be synchronized to each mating act.The involvement of medial preoptic neurons in sexual arousal, initial penile erection and that of dorsomedial hypothalamic neurons in the copulatory act are suggested by the present findings.     

Epilepsy syndromes associated with hypothalamic hamartomas.

PURPOSE: Hypothalamic hamartoma (HH) related epilepsy presents with gelastic seizures (GS), other seizure types and cognitive deterioration. Although seizure origin in GS has been well established, non-GS are poorly characterized. Their relationship with the HH and cognitive deterioration remains poorly understood. We analyzed seizure type, spread pattern in non-GS and their relationship with the epileptic syndrome in HH. METHODS: We documented all current seizure types in six adult patients with HH-epilepsy with video-EEG monitoring, characterized clinical-electrographic features of gelastic and non-gelastic seizures and correlated these findings with cognitive profile, as well as MRI and ictal SPECT data. RESULTS: Only four seizure types were seen: GS, complex partial (CPS), tonic seizures (TS) and secondarily generalized tonic-clonic seizures (sGTC). An individual patient presented either CPS or TS, but not both. GS progressed to CPS or TS, but not both. Ictal patterns in GS/TS and in GS/CPS overlapped, suggesting ictal spread from the HH to other cortical regions. Ictal SPECT patterns also showed GS/TS overlap. Patients with GS-CPS presented a more benign profile with preserved cognition and clinical-EEG features of temporal lobe epilepsy. Patients with GS-TS had clinical-EEG features of symptomatic generalized epilepsy, including mental deterioration. CONCLUSIONS: Video-EEG and ictal SPECT findings suggest that all seizures in HH-related epilepsy originate in the HH, with two clinical epilepsy syndromes: one resembling temporal lobe epilepsy and a more catastrophic syndrome, with features of a symptomatic generalized epilepsy. The epilepsy syndrome may be determined by HH size or by seizure spread pattern.     

Medial calcaneal neuropathy is associated with plantar fasciitis.

OBJECTIVE: To demonstrate a method of sensory nerve conduction study (NCS) for the medial calcaneal nerve (MCN) and confirm the medial calcaneal neuropathy in patients with plantar fasciitis (PF). METHODS: Twenty-six patients with clinical and ultrasonographic diagnosis of PF participated in the present study. An antidromic method for sensory NCS of MCN was performed in each patient and in 30 controls. The conduction latency, sensory nerve conduction velocity (SNCV) and amplitude of the sensory nerve action potential (SNAP) were measured and the correlation of the SNCV of MCN with both body weight and body mass index (BMI) was studied. RESULTS: The mean conduction latency obtained in the MCN was greater in the PF patients than in the normal controls. Mean SNCV and SNAP amplitude of the MCN were significantly less in the PF patients than in the normal controls. Body weight and BMI were greater in PF patients than in controls. Six patients were identified as having a medial calcaneal neuropathy by using the criteria of the lowest normal values of the NCS of MCN from the normal controls. CONCLUSIONS: Medial calcaneal neuropathy is associated with PF. The present method of sensory NCS is useful and objective in the diagnosis of the medial calcaneal neuropathy. SIGNIFICANCE: Medial calcaneal neuropathy was confirmed by the sensory NCS of MCN and shown to be associated with PF.     

Common side effects associated with monoamine oxidase inhibitors

There is relatively little documentation on the common side effects associated with monoamine oxidase inhibitors (MAOI) and their frequency of occurrence. A retrospective chart review of patient records in a Mood Disorders Service was completed. Side effects of patients receiving phenelzine (N = 42) and tranylcypromine (N = 19) were rated as mild (resulting in no change in treatment), moderate (some modification in treatment plan necessary), and severe (definite change in treatment plan or drug discontinuation due to MAOI side effect). A total of 35 reports of side effects were noted in 15 of 19 tranylcypromine patients (1.84 per patients) and a total of 125 side effect reports were noted in 39 of 42 phenelzine patients (2.98 per patient). Only two severe tranylcypromine side effects occurred (resulting in drug cessation for one of these patients - hypotension), while 9 severe reactions occurred with phenelzine, resulting in drug discontinuation in 6 of these patients. The side effects for tranylcypromine and the number of reports were insomnia (N = 10), sedation (N = 8), hypotension (N = 5), sexual dysfunction (N = 3), hypomania (N = 3), weight gain/edema (N = 2), hypertensive episode (N = 2), and myoclonic jerking (N = 2). The number of reports of phenelzine side effects were insomnia (N = 26), hypomania/mania (N = 27; most common reason for drug cessation - 4), hypotension (N = 16; three cases considered severe), weight gain/edema (N = 15), sedation (N = 15), sexual dysfunction (N = 13), hypertensive episode (N = 6), and myoclonic jerking (N = 7).(ABSTRACT TRUNCATED AT 250 WORDS)     

Distribution of type A and type B monoamine oxidase activity in hypothalamic nuclei of the rat.

The regional distribution of type A, type A and B and type B activity of monoamine oxidase (MAO) in individual nuclei of the rat hypothalamus was studied according to quantitative micromethods with clorgyline as a specific inhibitor of type A MAO. As results, type A and type B MAO were distributed differently in the rat hypothalamus. It is suggested that type B MAO acts differently from type A MAO in regard to the function of the hypothalamus.     

Callosotomy for generalized seizures associated with hypothalamic hamartoma

Abstract

A case is reported of intractable epilepsy associated with a hypothalamic hamartoma in an 18 year old man. The patient underwent a two-third anterior callsotomy and, subsequently, removal of the hamartoma. CaUosotomy did not affect the generalized seizure pattern. The authors believe this to be the first documented case of hypothalamic hamartoma in which callosotomy for seizure control was attempted. The poor response to callosotomy suggests the extracallosal diffusion of the generalized seizures from hypothalamic hamartomas. [Neurol Res 1993; 15: 139-141]     

Effects of intracerebroventricular angiotensin II and olfactory stimuli on multiple unit activity in preoptic and anterior hypothalamic areas: medial-lateral comparison

Under urethane anesthesia multiple unit activity (MUA) recordings were taken from medial and lateral preoptic and anterior hypothalamic sites in 21 rats during multiple dose intracerebroventricular (i.vt.) injections of angiotensin II (AII), using artificial CSF as control. Olfactory stimuli were also presented. Whilst lateral sites on average were significantly less responsive to AII than were medial sites, some of the former were very responsive. None of the 14 lateral sites that yielded an MUA response to AII failed to yield an MUA response to olfactory stimulation. On the other hand, 11 of 12 medial sites that yielded an MUA response to AII failed to yield an MUA response to olfactory stimulation. On the basis of these data it is suggested that the medial and lateral regions of the basal forebrain serve different functions, the former more related to internal sensing and the latter more related to integration of internal and external sensing. The findings are discussed in relation to the dual olfactory system and to theories of motivation.     

Choline acetyltransferase activity associated with cerebral cortical microvessels does not originate in basal forebrain neurons

Cerebral cortical microvessels are innervated by cholinergic fibers that are probably involved in the regulation of local cerebral blood flow and blood-brain barrier permeability. The possibility exists that the cholinergic terminals associated with the cortical microvasculature belong to neurons from the nucleus basalis magnocellularis (NBM), where 70% of the cortical cholinergic projections originate. To test this hypothesis, ibotenic acid (25 nmol) was injected unilaterally in the NBM in rats, and 14 days later, choline acetyltransferase (ChAT) activity was measured in the frontoparietal cortex and in a blood vessel fraction isolated from this region. Lesions of the NBM resulted in a 50% decrease of cortical ChAT as compared with control or sham-operated hemispheres; however, no changes were observed in the ChAT activity associated with cortical microvessels. These results indicate that, in rat cerebral cortex, the perivascular cholinergic terminals do not originate in the basal forebrain.     

Dementia associated with disorders of the basal ganglia

Dementia is now the leading cause of death in the United Kingdom, accounting for over 12% of all deaths and is the fifth most common cause of death worldwide. As treatments for heart disease and cancers improve and the population ages, the number of sufferers will only increase, with the chance of developing dementia doubling every 5 years after the age of 65. Finding an effective treatment is ever more critical to avert this pandemic health (and economic) crisis. To date, most dementia-related research has focused on the cortex and the hippocampus; however, with dementia becoming more fully recognized as aspects of diseases historically categorized as motor disorders (e.g., Parkinson's and Huntington's diseases), the role of the basal ganglia in dementia is coming to the fore. Conversely, it is highly likely that neuronal pathways in these structures traditionally considered as spared in Alzheimer's disease are also affected, particularly in later stages of the disease. In this review, we examine some of the limited evidence linking the basal ganglia to dementia.     

Acquired obsessive-compulsive disorder associated with basal ganglia lesions

The authors report 5 cases of acquired obsessive-compulsive disorder occurring later in life. Patients' presentations, which could be readily mistaken for a delusional disorder, were associated with depressive symptoms and basal ganglia lesions, implicating dysfunction of the cortical-basal ganglia-thalamic-cortical neuroanatomical circuit.     

Mycoplasma pneumoniae encephalitis associated with basal ganglia necrosis

IntroductionSevere central nervous system diseases, such as encephalitis, have been reported in association with Mycoplasma pneumoniae infections.Case reportA previously healthy 5-year-old boy presented with an atypical pneumonia; he rapidly developed encephalitis revealed by lethargy, generalized status epilepticus. MRI showed abnormal signals in the basal ganglia, typical of bilateral striatal necrosis. Serologic tests for M. pneumoniae were positive, the child recovered almost completely.ConclusionM. pneumoniae infection should be considered in all cases of acute encephalopathy; yet the pathogenesis of the disorder is unknown and the treatment uncertain.     

A case of hypothalamic hamartoma associated with arachnoid cyst

A 14-year-old girl presented with seizures. Radiological examinations revealed an arachnoid cyst in left middle fossa and a cystic mass in the interpeduncular cistern. The cyst was opened and the wall of the cyst and a mass were biopsied. The histological findings were characteristic of an arachnoid cyst and hamartoma, respectively. A hypothalamic hamartoma associated with an arachnoid cyst is comparatively rare; however, such a case may help clarify the genesis of this malformation. Received: 5 November 1998 Accepted: 19 January 1999     

Functional brain mapping of ictal activity in gelastic epilepsy associated with hypothalamic hamartoma: A case report

Hypothalamic hamartomas (HHs) have been demonstrated as the cause of gelastic epilepsy, both by intracranial electrodes and functional imaging. The neocortex becomes secondarily involved, through poorly characterized propagation pathways. The detailed dynamics of seizure spread have not yet been demonstrated, owing to the limited spatial–temporal resolution of available functional mapping. We studied a patient with epilepsy associated with HH and gelastic epilepsy. Simultaneous electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) of several seizure events were obtained, with blood oxygen level dependent (BOLD) activation of the hamartoma, and left hemisphere hypothalamus, hippocampus, parietal–occipital area, cingulate gyrus, and dorsal–lateral frontal area. Integration of regional BOLD kinetics and EEG power dynamics strongly suggests propagation of the epileptic activity from the HH through the left fornix to the temporal lobe, and later through the cingulate fasciculus to the left frontal lobe. The EEG/fMRI method has the spatial–temporal resolution to study the dynamics of seizure activity, with detailed demonstration of origin and propagation pathways.