[Splenic irradiation: apropos of 8 cases. Clinical indications and literature review]. / Radioterapia esplénica: a próposito de 8 casos. Indicaciones y revisión de la literatura.

Clinical indications of splenic irradiation in haematological disorders include the irradiation in lymphoproliferative disorders with spleen infiltration, palliative treatment of splenomegaly in malignant diseases like chronic lymphocytic leukaemia or myeloproliferative disorders, with the purpose of relief from abdominal pain associated with capsular enlargement size and decrease cytopenias secundaries to hypersplenism.This paper reports our experience with spleen irradiation in the Hospital General Universitario Gregorio Marañón in the last five years, and analyzes indications, results and toxicity, and an actual review of the literature.

Radioterapia esplénica: a propósito de 8 casos. Indicaciones y revisión de la literatura / Splenic irradiation: a proposal of 8 cases. Clinical indications and literature review

Las indicaciones de la radioterapia (RT) esplénica en los desórdenes hematológicos incluye la irradiación del bazo en aquellos procesos linfoproliferativos, que cursan con infiltración del mismo, el tratamiento paliativo de la esplenomegalia en las enfermedades malignas como la leucemia linfoide crónica o los síndromes mieloproliferativos, que cursan con dolor por la distensión capsular del bazo, y las citopenias secundarias al hiperesplenismo. En este trabajo presentamos la experiencia acumulada en el tratamiento de la esplenomegalia con RT del Hospital General Universitario Gregorio Marañón en los últimos 5 años, analizando sus indicaciones, resultados y toxicidad así como una revisión actualizada de la literatura

Clinical indications of splenic irradiation in haematological disorders include the irradiation in lymphoproliferative disorders with spleen infiltration, palliative treatment of splenomegaly in malignant diseases like chronic lymphocytic leukaemia or myeloproliferative disorders, with the purpose of relief from abdominal pain associated with capsular enlargement size and decrease cytopenias secundaries to hypersplenism. This paper reports our experience with spleen irradiation in the Hospital General Universitario Gregorio Marañón in the last five years, and analizes indications, results and toxicity, and an actual review of the literature

Anorectal function in patients with complete rectal prolapse. Differences between continent and incontinent individuals.

AIMS: A study is made of the alterations in anorectal physiology among rectal prolapse patients, evaluating the differences between fecal continent and incontinent individuals. PATIENTS AND METHODS: Eighteen patients with complete rectal prolapse were divided into two groups: Group A (8 continent individuals) and Group B (10 incontinent women), while 22 healthy women were used as controls (Group C). Clinical exploration and perineal level measurements were performed, along with anorectal manometry, electrophysiology, and anorectal sensitivity to electrical stimuli. RESULTS: The main antecedents of the continent subjects were excess straining efforts, while the incontinent women presented excess straining and complex deliveries. Pathological perineal descent was a frequent finding in both groups, with a hypotonic anal canal at rest (p < 0.001 vs controls) and at voluntary squeezing (p < 0.001 vs controls). In turn, the incontinent patients exhibited a significantly lower anal canal pressure at rest than the continent women (p < 0.05). There were no significant differences between Groups A and C in terms of pudendal motor latency, though latency was significantly longer in Group B than in the controls (p < 0.01). Moreover, pudendal neuropathy was more common, severe and often bilateral in Group B. There were no differences in rectal sensation to distention or in terms of the volumes required to relax the internal anal sphincter. In turn, both prolapse groups exhibited diminished anal canal and rectal sensitivity to electrical stimuli. CONCLUSIONS: Patients with rectal prolapse exhibit a hypotonic anal canal at rest, regardless of whether they are continent to feces or not. Continent patients have less pudendal neuropathy and therefore less pressure alterations at voluntary sphincter squeeze than incontinent individuals.

Anorectal sensitivity in patients with obstructed defaecation.

Patients with obstructed defaecation (OD) perform major defaecatory efforts that lead progressively to pudendal motor neuropathy. Anorectal sensory function in these patients and its possible influence in the pathogenesis of the disease have been little studied. In the present paper we investigated anorectal sensitivity to electric and thermal stimuli in patients with OD, and studied the possible existence of pudendal sensory neuropathy associated to their known pudendal motor neuropathy. Forty subjects were divided into two groups: 21 healthy controls (11 females and 10 males; mean age 51.8 +/- 11 years, range 33-67) and 19 patients with OD (18 females and 1 male; mean age 48 +/- 15 years, range 20-71). The patients with OD suffered constipation and an obstruction sensation upon defaecating, even in the case of soft stools. Clinical perineometry, manometry, pudendal motor latency studies, external anal sphincter single fibre electromyography and the evaluation of sensitivity to electric and thermal stimuli were carried out in all cases. All pudendal motor function parameters showed statistically significant differences between the two groups. In the controls the electrical sensitivity threshold was minimal in the mid anal canal, where sensory receptor presence is greater. Sensitivity was significantly higher in the upper and lower anal canal regions (P < 0.05), and much higher in the rectum (P < 0.001). A similar sensory profile was recorded in the patients with OD, though with significantly higher thresholds at all points with respect to the controls. The thermal stimulus thresholds in the lower and middle anal canal were significantly smaller than in the upper canal region and rectum, and the thresholds were again higher among the patients with OD than among the controls. In all cases the thresholds for heat were lower than for cold stimuli. In both groups the motor function parameters were correlated with the sensory function variables, and the latter between themselves. Patients with OD presented sensory deterioration at all points studied in the anal canal and rectum. Sensory pudendal neuropathy was found to be associated with the pudental motor neuropathy.

Somatosensory evoked potentials and central motor pathways conduction after magnetic stimulation of the brain in diabetes.

Somatosensory evoked potentials (SEPs) on stimulating median and posterior tibial nerves, and central and spinal conduction time of the motor pathways calculated by means of magnetic stimulation of the cortex were valuated in diabetic patients. The latencies L1-Cortex and L1-C7 were significantly larger in 54 diabetics than in controls. An increment in L1-C7 interval was found in 17 patients, and the latency L1-Cortex was increased in 20. No patients showed increase in C7-Cortex interval. The increased latency L1-C7 reflects a delayed conduction along afferent spinal pathways in some patients with diabetes in contrast with the normal C7-Cortex supraspinal segment. The central and spinal conduction time after magnetic stimulation of the cortex were normal in 14 out of 15 tested diabetics suggesting that central motor pathways were spared. These results are consistent with the existence of a central-peripheral sensory axonopathy in some diabetics.

Transcranial magnetic stimulation in multiple system and late onset cerebellar atrophies.

Central motor conduction time (CMCT) after transcranial magnetic stimulation (TMS) of the cortex, electromyography and nerve conduction velocity were performed in 24 patients with multiple system (MSA) and late onset cerebellar atrophy (LOCA) (often olivopontocerebellar atrophy--OPCA -). CMCT was abnormal in 7 patients with OPCA and one with LOCA. CMCT abnormalities (43% of cases) and increased threshold (68%) were more often found within OPCA group than in another multisystem atrophy and LOCA. Reduction in amplitude of the response after TMS was significantly correlated with cerebral hemispheres's atrophy. Increased threshold was correlated with upper vermal hemisphere atrophy and enlargement of the fourth ventricle. Electrophysiologic signs of mixed peripheral neuropathy were found in 8 patients. TMS abnormalities were not related to peripheral nerve involvement. Marked variation in CMCT suggests heterogeneity in these diseases. However, the percentage of CMCT abnormalities in OPCA group suggests that TMS seems to play a role in the neurophysiological diagnosis of these heterogeneous disorders.

Prevalence of pudendal neuropathy in fecal incontinence. Results of a prospective study.

PURPOSE: A prospective study was made of the prevalence and associations of pudendal neuropathy in 96 patients with fecal incontinence (72 females and 24 males). METHODS: Clinical exploration, perineal level measurement, anorectal manometry, and electrophysiologic evaluations (pudendal nerve terminal motor latency (PNTML) and external sphincter fiber density (FD)) were performed. RESULTS: Pudendal neuropathy (defined as PNTML > 2.2 ms or FD > 1.65) was found in 67 patients (69.8 percent) and was more common in females (75 percent) than in males (50 percent; P = 0.05). Pudendal neuropathy was also more frequent in patients with pathologic perineal descent (85 percent vs. 55 percent; P < 0.01) or exhibiting risk factors such as difficult labor or excessive defecatory straining (P < 0.01). Perineal level at staining correlated inversely with both PNTML and FD (P < 0.01). Manometric findings suggested greater external anal sphincter damage in patients with pudendal neuropathy than in those suffering fecal incontinence but no neuropathy (P < 0.05). Pressure caused by the striated anal sphincter was also inversely correlated to PNTML. Pudendal neuropathy was encountered in 37 of 33 (58.7 percent) patients with sphincter injury vs. in 31 of 33 (93.9 percent) patients with idiopathic fecal incontinence (P < 0.01). CONCLUSIONS: Pudendal neuropathy is an etiologic or associated factor often present in patients with fecal incontinence. In this sense, clinical, perineometric, and manometric findings correlate with pudendal neuropathy, though such explorations do not suffice to detect it.

Electrophysiologic study in peripheral neuropathy associated with HIV infection.

Clinical and electrophysiologic features in 22 patients with HIV infection are reported. Four cases had chronic demyelinating polyneuropathy, two mononeuropathy multiplex, and nine symmetrical sensory-motor polyneuropathy. Seven cases had normal clinical and electromyographic examination. Electrophysiological study had a higher diagnostic yield (68%) than clinical examination (50%) for peripheral neuropathy diagnosis. Thus, peripheral nerve abnormalities are frequent in patients with different stages of HIV infection, although their pathogenesis remains unclear. Symmetrical sensory-motor polyneuropathy is the main type of neuropathy seen in ouvert AIDS, whereas chronic demyelinating polyneuropathy was mainly diagnosed in patients with asymptomatic HIV infection as first manifestation of the disease. Axonal or demyelinating nerve damage was established according to electrophysiological criteria. Frequently a mixture of both lesions was found. Electrophysiologic study is also a good index of neuropathy evolution in HIV infection and to follow-up of nerve abnormalities after treatment.

Chronic inflammatory demyelinating polyneuropathy as first manifestation of human immunodeficiency virus infection.

We studied three patients who were admitted to the hospital because of progressive weakness without other systemic signs or symptoms. All three cases were young males who had been intravenous drug user for many years. Electrophysiologic study showed prolonged distal latencies and marked slowing of motor and sensory conduction velocities, consistent with primary demyelination. Nerve biopsy also showed signs of demyelination. Antibodies against HIV in CSF and blood were detected during the diagnostic evaluation. Clinical and electrophysiological studies improved in two cases after prednisone administration. Patients with predominant motor demyelinating neuropathies and risk factors should be screen for HIV infection.

[Peripheral neuropathy in HIV infection]. / Neuropatía periférica en la infección por VIH.

Neuropathy may complicate all stages of human immunodeficiency virus infection (HIV). Different types of peripheral neuropathy and myelopathy have been reported associated with HIV infection: sensory symmetrical polyneuropathy, acute inflammatory demyelinating polyneuropathy, chronic inflammatory demyelinating polyneuropathy, mononeuropathy multiplex, sensory ataxic neuropathy (ganglioneuronitis), cauda equina syndrome, amyotrophic lateral sclerosis, spastic paraparesia, and subclinical neuropathy diagnosed by electrophysiologic study. We describe the main clinical, electrophysiological and pathological features in these different types of neuropathy and comment their pathogenesis and treatment. Results in our series of twenty-two patients are also reported. In this series we want to underline three cases in which a chronic demyelinating polyneuropathy was the first manifestation of HIV infection. Thus, patients with predominantly motor demyelinating neuropathies and suspicious risk factors should be screened for silent HIV infection.