Search

Tension-type headache is a very common disease with a high socio-economic impact as its lifetime prevalence is 30-78% in the general population. The incidence of inflammatory bowel diseases is continuously rising. Limited data are accessible on quality of life in patients with surgically treated ulcerative colitis. The aim of our study is to examine quality of life, concerning headache, among patients who had undergone surgery due to ulcerative colitis.Between 1 January 2005 and 1 March 2016, surgery was performed due to ulcerative colitis in 75 patients. During this retrospective analysis the average duration of the follow-up was 46 (1-124) months. The pre-sence of headache was evaluated by the use of Brief Illness Perception and Headache Questionnaires.Among the primary headache disorders (n=27), tension-type headache occurred in 19 (70.4%) cases, and 8 (29.6%) patients had migraine (without aura). Among tension-type headache cases 17 (89.5%) patients experienced episodic form and 2 (10.5%) suffered from chronic form. Patients with headache had obtained a significantly higher score on Brief Illness Perception Questionnaire.According to our study tension-type headache is common among patients with ulcerative colitis. This observation raises the question whether stress plays role in the pathogenesis of both diseases, which influences and worsens considerably quality of life. Neurological examination, psychological and psychiatric guidance are worth considering in patients with ulcerative colitis.A tenziós típusú fejfájás igen gyakori, az átlagpopulációban az élettartam-prevalenciája 30-78%, így meglehetősen magas a társadalmi-gazdasági hatása. A gyulladásos bélbetegségek incidenciája folyamatosan emelkedik. Magyarországon colitis ulcerosa miatt műtéttel kapcsolatos életminőségi adatokkal eddig limitált számban rendelkeztünk. Jelen tanulmányunkban a colitis ulcerosa miatt műtéten átesett betegpopuláció életminőségét vizsgáltuk a fejfájás vonatkozásában.2005. január 1. és 2016. március 1. között 75 betegnél végeztünk colitis ulcerosa miatt műtétet. Retrospektív módszerrel végzett utánkövetésünk átlagosan 46 (1-124) hónapig tartott, mely során a Rövid Betegségpercepció Kérdőívet és a Fejfájás Kérdőívet felhasználva regisztráltuk a fejfájás megjelenését.Az elsődleges fejfájásbetegségek (n=27) közül 19 (70,4%) beteg tenziós típusú fejfájásban, 8 (29,6%) beteg migrénben (aura nélküli) szenvedett. A tenziós típusú fejfájásos betegek közül 17 (89,5%) epizodikus, 2 (10,5%) krónikus formába tartozott. A fejfájástól szenvedő betegek szignifikánsan magasabb pontszámot értek el a Rövid Betegségpercepció Kérdőíven.Felmérésünk szerint a tenziós típusú fejfájás a colitis ulcerosában szenvedő betegek között gyakori. Ez felveti a két kórforma között a stressznek mint kóroki tényezőnek a szerepét, mely nagymértékben befolyásolja és rontja a betegek életminőségét. A fentiek alapján megfontolandó a colitis ulcerosában szenvedő populáció neurológiai kivizsgálása, szükség szerint pszichiátriai, pszichológiai gondozása.

The present work is based on literature data from PubMed. Neuropathic pain is caused by a lesion or disease of the somatosensory system. Peripheral and central sensitization play a crucial role in its pathomechanism. The clinical symptoms are mainly characterized by burning and throbbing pain and sensory disturbances like hyperalgesia and allodynia. Therapeutic recommendations are antidepressants, antiepileptics, opioids and neuro-stimulation methods.

Amyotrophic lateral sclerosis is an idiopathic, utlimately fatal disease, clinically manifest as progressive weakness and spasticity, associated with the loss of motoneurons. Circumstantial evidence supports a role for autoimmune processes in the progression of this human disorder. Two immune-mediated animal models have been developed in our laboratory for motor neuron loss. Experimental autoimmune motor neuron disease is a lower motor syndrome induced in guinea pigs by the repeated injection of a purified bovine spinal motor neuron antigen. Affected animals demonstrate extremity weakness, associated with electromyographic and morphologic evidence of denervation, a loss of spinal cord motor neurons, high antibody titers against motor neurons, and localization of IgG immunoreactivity to the neuromuscular junction and motor neuron cytoplasm. Experimental autoimmune grey matter disease is a more acute and severe disorder involving both upper and lower motor neurons, induced in guinea pigs by inoculation of a bovine ventral spinal cord homogenate, in which scattered foci of denervation are observed in the motor cortex and ventral spinal cord. Similarities between these diseases and human ALS are reviewed.

Guinea pigs inoculated with bovine spinal cord ventral horn homogenate develop a syndrome termed experimental autoimmune gray matter disease (EAGMD) characterized by extremity weakness, bulbar signs, and a loss of lower and upper motoneurons. To provide evidence for the role of autoimmune mechanisms, we have administered the immunosuppressant cyclophosphamide prior to and after gray matter immunization. Pretreatment with cyclophosphamide prevented the appearance of clinical signs of disease and decreased the loss of spinal cord motoneurons, the appearance of damaged motoneurons, and the antibody titer to motoneurons. Treatment 7 days after immunization attenuated the expression of disease. Treatment immediately after signs also improved the clinical and pathological findings. In all cyclophosphamide-treated animals there was less IgG within motoneurons and less inflammation. These results support the role for autoimmune mechanisms in motoneuron loss and degeneration in EAGMD.

Endothelin is a potent peptide mediator that is synthesized by a number of cells. Previous studies have revealed the occurrence of endothelin in nerve cell bodies of some peripheral ganglia. Endothelin mediates its effects via two distinct receptor subtypes ETA and ETB. The present study was designed to investigate the presence of these two receptors in the human trigeminal ganglion.Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to show the presence of mRNA encoding ETA and ETB receptors in the human trigeminal ganglion. To localize the protein immunocytochemistry with antibodies against the endothelin receptors was used.Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed mRNA for both receptor subtypes in the human trigeminal ganglion. Immunocytochemistry revealed numerous cell bodies containing the ETA and the ETB receptor proteins.The expression of ETA and ETB receptors in the human trigeminal ganglion suggests a role for endothelin in autonomic and sensory neural transmission.

The purpose of this study was to localize in cranial ganglia of man the occurrence of the putative gaseous neural messenger carbon monoxide (CO) and the biliverdin degrading enzyme biliverdin reductase (BVR).Immunocytochemistry with antibodies against the CO-inducing enzymes HO-1, HO-2, BVR and calcitonin gene-related peptide was used.In the trigeminal ganglion about 60% of the cell bodies exhibited HO-2- and about 40% BVR-immunoreactivity. HO-2- as well as BVR-immunoreactivity was predominantly (78%) expressed in medium-sized cells (30-60 microm). In the superior cervical ganglion about 40% of the cell bodies exhibited HO-2-immunoreactivity. In the sphenopalatine and otic ganglia only a few cell bodies were HO-2 immunoreactive. HO-1, the inducible isoform of heme oxygenase, gave only very weak immunoreactivity in all ganglia examined. Double immunostaining revealed that in the human trigeminal ganglion HO-2 and BVR co-localized with calcitonin gene-related peptide.The finding suggests that CO might serve as a modulator of synaptic transmission in man.

• Objective. —Immunohistochemical examination was undertaken to assess the presence of lymphocytes and lymphocyte subsets in the spinal cord in amyotrophic lateral sclerosis (ALS). Design. —Twenty-seven consecutive ALS autopsy cases and 11 consecutive disease—control autopsy cases were examined. Tissue sections were reacted with mouse monoclonal antibody to human leukocyte common antigen, or monoclonal antibody to human B-cell L26 antigen, and detected with immunoperoxidase techniques. Unfixed sections were reacted with antihuman Leu-3a and Leu-3b/CD4 or antihuman Leu-2a/CD8 mouse monoclonal antibody and then detected with peroxidase techniques. Setting. —Tertiary care hospital. Cases. —Amyotrophic lateral sclerosis and non-ALS control autopsy specimens. Main Outcome Measure. —Detection of lymphocytes by histological and immunohistochemical reactivity. Results. —Perivascular and intraparenchymal lymphocytic infiltrates were found in the spinal cord of 18 of 27 consecutive ALS autopsy cases. The lymphocytes possessed only T-cell markers; no B-cell markers could be demonstrated. T-helper cells were found in proximity to degenerating corticospinal tracts, while T-helper and T-suppressor/cytotoxic cells were demonstrated in ventral horns. Lymphocytes were present in the spinal cord of only one control specimen (multiple sclerosis) and in none of the remaining 10 control specimens. In ALS tissue, the lymphocytic infiltrates did not correlate with the rate of progression or stage of the disease or with the presence or absence of terminal infections. Conclusions. —T-cell lymphocytes are present in the spinal cord of patients with ALS. T-helper cells are found in proximity to corticospinal tract degeneration, while T-helper and T-suppressor/cytotoxic cells are present in ventral horns. The role of these lymphocytes remains to be elucidated.