Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hypesthesia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1989

[Tunica vaginalis autografting in Peyronie's disease].

Surgical excision of the indurated penile plaque and tunica vaginalis autografting was done in 3 patients. Preoperatively, their chief complaints had not been impotence but penile angulation or pain. Postoperatively, all of them improved and erectile failure was not seen, although hypesthesia of glans developed in all patients. One patient complained of impotence. The patients had been followed from 2 months to 9 months. As prosthesis is not prevailing in Japan and tunica vaginalis is easy to procure and handle, tunica vaginalis autografting is recommended.

Aged↗
PubMed1989

[Paresthetic notalgia. Report of 2 cases].

The Authors describe two cases of notalgia paresthesica, a disorder with localized pruritus of the back and hypesthesia for touch possibly due to a sensory neuropathy involving the posterior primary rami of thoracic nerve T2 through T6. The condition is not rare, but underdiagnosed for the poor clinical relevance. The possible X-linked hereditary transmission and other pathogenetic hypotheses are discussed.

Back↗
PubMed1986

Congenital corneal anisohypesthesia: report of a case.

A neuroparalytic ulcer developed only in the right eye of a three-year-old girl with bilateral congenital corneal hypesthesia. The central parts of the cornea in both eyes were practically isohypesthetic, but there was a marked difference in sensitivity in the peripheral zones of the right and left cornea. Presumably there was sufficient peripheral antidromic activity of the sensory nerves in the left cornea to prevent the development of a neuroparalytic ulcer.

Child, Preschool↗
PubMed1985

[Cheiro-oral syndrome with pontine infarct--report of a case].

A case of cheiro-oral syndrome presumably due to brain stem infarction was reported. A 41-year-old man suddenly experienced the numbness of the palm and the lips on the left side at 2 p. m. March 30, 1982 and was admitted to our clinic at 5 p.m. on that day. Neurological examination on admission revealed hypesthesia of the palm and the lips on the left side, but pain and temperature sensibilities were preserved. Neither astereognosia nor extinction phenomenon was there. CT scan showed no abnormal findings. At 9 p.m. his speaking became somewhat obscure and he became unable to swallow fluid. And after ten hours or so, he became quadriplegic, anarthric and lost almost all voluntary movement below the eye, while his consciousness was preserved ("Locked-in" syndrome). CT scan taken on the 9th hospital day revealed brain stem infarction. He expired on the 58 th hospital day because of the exacerbation of pneumonia. At autopsy both vertebral arteries and basilar artery were markedly sclerotic. The rostral two-thirds of the basilar artery was occluded by organized thrombus. The serial microscopic sections through the midbrain and the medulla oblongata showed extensive infarction of the basis pontis. The tegmentum pontis remained free, except that a small offshoot of the infarct reached into the medial part of the medial lemniscus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Chronic pain and syringomyelic slit of the posterior horns of the spinal cord].

Two male patients 46 and 44 y.o. respectively, were admitted for a syndrome of chronic pain characterized by: sudden onset, spontaneous or following spasmodic coughing, of an anterior hemithoracic pain slowly progressing to involve several unilateral cervicothoracic dermatomes, a continuous burning sensation made worse by light touch, limb movements and cold water, and partially relieved by warm water or deep palpation. On examination, patient 1 revealed no sensorimotor deficit after repeated observations during 8 years. At autopsy, a syrinx localized at the cord segments corresponding to the symptoms was found without documentation of specific causal factors. It involved the posterior horn of the cord selectively. In patient 2, pain was associated with slight hypesthesia to pinprick and heat from C2 to T5 on the left without motor deficit since 18 months. A high resolution C.A.T. scan showed an intramedullary cavity 0.3 cm from the midline in the projection of the posterior horn without anomalies at the cervicomedullary junction. These observations link chronic pain syndromes with predominantly posterior horn lesions, which so far have failed to respond to conventional therapeutic measures.

Adult↗
PubMed1994

Tegmental pontine hemorrhage with pure trigeminal motor impairment.

We report a patient with a right dorsolateral pontine syndrome including right masticatory weakness without facial hypesthesia. Brain computed tomography showed a right dorsolateral pontine hemorrhage. Blink reflex study indicated preservation of spinal tracts and sensory nuclei of the trigeminal nerve. Right masseter electromyography revealed denervation. This patient provides a good correlation between clinical, radiological and electrophysiological findings and nuclear organisation of the trigeminal nerve.

Aged↗
PubMed1993

[Cervical myelopathy as complication of manual therapy in a patient with a narrow cervical canal].

A 31-year-old man had manipulative therapy because of pain in the neck, the left shoulder and the left arm. Immediately after cervical traction he developed neurological symptoms. Clinical investigation led to the diagnosis of cervical myelopathy. The patient had a rather narrow cervical canal. Six weeks after treatment with external fixation and corticosteroids the situation had improved markedly, with remaining hypesthesia in both hands and the right leg.

Adult↗
PubMed1996

[Polyneuropathy, diarrhea].

A 44-year-old patient with 24 kg reduction of body weight within three years due to recurrent diarrhea was admitted to the hospital. Physical findings of the patient were not remarkable, except for hypesthesia and hypalgesia of the front of the tibia and of the lower legs. Laboratory as well as endoscopic and functional examinations of the gastrointestinal tract did not reveal any remarkable finding. Infectious origins of the disease were excluded. A histological examination of a rectum specimen yielded amyloid deposits in the submucosa of the rectum. In the family history of the patient, relatives with liver and gastrointestinal diseases due to amyloidosis were detected. Amyloid deposits and the positive family history of the patient led to the diagnosis of a gastrointestinal manifestation of familial amyloidosis.

Adult↗
PubMed1976

Painful diabetic neuropathy. A morphometric study.

We investigated three diabetic patients whose neuropathy was characterized by pain, hypesthesia, and autonomic dysfunction, with preservation of epicritic sensation and muscle-stretch reflexes. Two sural nerves were studied qualitatively and quantitatively, using teased fiber, light, and electron microscopical techniques. The most striking alterations were encountered in unmyelinated and small myelinated fibers. Unmyelinated nerve fiber sprouting was evident. The clinical features, which suggested small-fiber involvement, correlated with the pathological findings in biopsied cutaneous nerve. The balance of evidence indicates that the painful small-fiber neuropathy of diabetes is an axonal disorder.

Adult↗
PubMed1982

Optic neuropathy and paratrigeminal syndrome due to Aspergillus fumigatus.

Chronic Aspergillus meningitis and cerebral vasculitis occurred in a 67-year-old man. He experienced periorbital pain that increased in severity during a ten-month period. Although no focal neurologic deficits were initially present, oculosympathetic paresis, corneal hypesthesia, and optic neuropathy developed. This is the first report, to our knowledge, of paratrigeminal syndrome with optic neuropathy due to aspergillosis. The case was also unusual because it was chronic and there was no extracerebral infection or predisposing factors, such as underlying malignancy or collagen vascular disease.

Aged↗
PubMed2000

Aspiration subsequent to a pure medullary infarction: lesion sites, clinical variables, and outcome.

BACKGROUND: Aspiration as a symptom of dysphagia and its apparent sequela, aspiration pneumonia, are common consequences of a stroke in the medulla. Previous reports that focused on dysphagia due to a medullary lesion were studies of single cases or a relatively small number of patients with multiple lesion loci. Moreover, the interval between the onset of stroke and the evaluation time of swallowing was not controlled and varied largely among patients. Thus, prediction of the swallowing status of patients with a medullary lesion has not been tenable. OBJECTIVES: To investigate the relation between the loci of pure medullary lesions and aspiration, to examine swallowing function over time, and to explore clinical variables that can predict aspiration. METHODS: We investigated 23 patients with pure medullary infarctions using the videofluoroscopic swallowing study and compared the airway status findings with the lesion location as determined with magnetic resonance imaging. The patients were classified by 6 medullary lesion-level categories (lower, lower-middle, middle, lower-middle-upper, middle-upper, and upper) and by 5 intralevel lesion loci (inferior-dorsal, large inferior-dorsolateral, para-median, midlateral, and dorsolateral). From the results of the videofluoroscopic swallowing studies, 2 patient groups were formed: one with aspiration and the other without aspiration. The clinical variables related to aspiration and outcome measures were also explored. RESULTS: Ten (44%) of the 23 patients manifested aspiration on swallowing: 9 (69%) of 13 with only middle-level lesions or lesions in multilevels, including the middle level; 1 (33%) of 3 with only upper-level lesions; and 0 (0%) of 7 with only lower-level medullary lesions. A lesion running the length of the middle and the lower medullary levels always resulted in aspiration. When an upper-level lesion was additionally involved, the incidence of aspiration depended on the horizontal extension of the lesion. We were able to discriminate the 2 patient groups with 95.7% accuracy using such variables as dysphonia, soft palate dysfunction, and facial hypesthesia. Most of the patients with aspiration symptoms due to a pure medullary infarction recovered rather quickly. CONCLUSIONS: Medullary infarctions often cause aspiration, but the occurrence may depend on the levels along the neuraxis and intralevel lesion loci. When different lesion levels and loci and their related clinical findings are considered as possible variables, aspiration becomes predictable. The outcome data prove that systematic control of evaluation time of swallowing was critical as we engaged in this study, since many aspirators with pure medullary infarctions resolve their swallowing difficulties rather quickly.

Adult↗
PubMed2001

Linear pontine trigeminal root lesions in multiple sclerosis: clinical and magnetic resonance imaging studies in 5 cases.

BACKGROUND: Magnetic resonance imaging (MRI) is useful for demonstrating demyelinating lesions in patients with multiple sclerosis (MS). Magnetic resonance imaging studies show that MS lesions are generally not uniform in shape, size, or distribution. Linearly shaped lesions at the trigeminal root entry zone have been occasionally reported in single cases of MS, but, to our knowlege, the frequency and the clinical features of such patients have not been comprehensively characterized. OBJECTIVE: To describe the frequency and the clinical and laboratory features of patients with MS who had linearly shaped lesions at the trigeminal root as seen on MRI. DESIGN AND SETTING: A retrospective review of medical records and MRI films of Japanese patients with MS admitted to a university hospital and its affiliated hospital in Sendai, Japan. PATIENTS AND METHODS: Brain MRI films of 74 consecutive Japanese patients with MS (51 females and 23 males) were studied retrospectively and the clinical and laboratory features of the patients with linearly shaped lesions at the trigeminal root were also investigated retrospectively. RESULTS: Five patients (6.8%) were shown to have T1-weighted-hypointense, T2-weighted-hyperintense, nonenhanced linear lesions in the pons on MRI, and these were uniformly localized in the intramedullary portion of the trigeminal root. All of these patients had clinically definite MS and had various types of facial sensory disturbances, such as neuralgia (1 patient), hypesthesia (2 patients), or paresthesia (3 patients). No other clinical or laboratory feature was characteristic in these 5 patients. CONCLUSIONS: Linear pontine trigeminal root lesions were common in our patients with MS. They were associated with various facial sensory symptoms. Since similar lesions are formed in animal models of herpes simplex virus infection, further study is needed to clarify whether these MS lesions are virally induced.

Adolescent↗
PubMed2002

Creutzfeldt-Jakob disease with amyotrophy and demyelinating polyneuropathy.

OBJECTIVE: To report the clinical and neuropathological features in a patient with Creutzfeldt-Jakob disease with amyotrophy and demyelinating polyneuropathy. DESIGN: Case report. PATIENT AND RESULTS: A 62-year-old man had progressive numbness of the left foot, unsteady gait, diminished deep reflexes, fasciculations, and tactile hypesthesia on the feet. Cerebrospinal fluid, electroneurography, and electromyography were suggestive of chronic inflammatory demyelinating polyneuropathy. He was treated with plasmapheresis, corticosteroids, and immunglobulins, with minimal improvement. After 2 months, severe amyotrophy, polyneuropathy, cerebellar signs, and dementia developed, and he died 8 months after onset of the disease. Autopsy and prion protein immunohistochemistry proved typical Creutzfeldt-Jakob disease. No mutation was found in the prion protein gene, and the codon 129 polymorphism was methionine-valine. In the ventral horn, the loss of the motoneurons was accompanied by prion protein immunoreactivity. The peripheral nerves were segmentally demyelinated but free of prion protein deposition. CONCLUSIONS: The view that peripheral neuropathy and amyotrophy may occasionally be an integral part of Creutzfeldt-Jakob disease is supported by our case, which showed these abnormalities simultaneously. These symptoms, when prominent, may cause problems in differential diagnosis.

Brachial Plexus Neuritis↗
PubMed1989

Surgical management of nasopharyngeal angiofibroma involving the cavernous sinus.

Involvement of the cavernous sinus by juvenile nasopharyngeal angiofibroma represents a therapeutic challenge. We present our experience over the past 5 years with the surgical management of six cases of juvenile nasopharyngeal angiofibroma involving this site. Three of six patients had involvement of the medial aspect of the cavernous sinus and tumor was removed using a midline extracranial approach. Of three remaining patients, two had invasion of the medial and inferior margin of the cavernous sinus and one represented a recurrent lesion. The tumor in these three cases was resected using a combined frontotemporal and lateral infratemporal fossa approach. An extracranial recurrence occurred in one patient, and the remaining five patients have had no evidence of recurrent disease 12 to 71 months following surgery. Morbidity has been limited to trismus, facial hypesthesia, and serous otitis media.

Adolescent↗
PubMed1997

Dejerine-Sottas neuropathy in mother and son with same point mutation of PMP22 gene.

We studied a 25-year-old black woman with healthy parents and her 2-year, 11-month-old son. Her motor development was delayed and she started to walk with support when she was 6 years old. She never walked independently and had always used a wheelchair. Neurological evaluation showed severe weakness and atrophy of her feet, legs, and hands, bilateral pes cavus and hammertoes, corrected scoliosis, hypesthesia for proprioception and vibration sense in both feet and ankles, and areflexia. She had normal intelligence. Her son also had delayed motor milestones and was still unable to stand and walk independently at almost 3 years. Neurological evaluation revealed diffuse muscle hypotonia and weakness with generalized areflexia and normal intelligence. No muscle atrophies or feet deformities were noticed. Nerve conduction velocities showed significant slowing (less than 5 m/s) with prolonged distal latencies (above 30 ms). Compound motor action potential amplitudes were markedly reduced. Electromyography revealed polyphasic motor unit potentials. Molecular genetic studies indicated a Trembler type missense point mutation of exon 4 of the peripheral myelin protein 22 gene that led to the substitution of a spartic acid for glycine in both the mother and her son. Her parents showed normal DNA studies.

Adult↗
PubMed1997

Severe Charcot-Marie-Tooth neuropathy type 1A with 1-base pair deletion and frameshift mutation in the peripheral myelin protein 22 gene.

A 27-year-old man with negative family history and both parents with normal neurological evaluation and motor nerve conduction velocities (MNCVs) showed onset of severe weakness of feet at 4 years of age. Subsequently he developed left equinovarus deformity, thoracic scoliosis, ulnar nerve enlargement, areflexia, distal hypesthesia and slowing of MNCVs for median and ulnar nerves (15-25 m/sec). Molecular genetic studies showed deletion of one nucleotide (G330) (codon 94) in exon 3 of the PMP22 gene associated with frameshift mutation.

Adult↗
PubMed1998

The role of axonal ion conductances in diabetic neuropathy: a review.

Diabetic neuropathy is a common complication in diabetes mellitus. Diabetic neuropathy is accompanied by alterations in axonal excitability, which can lead to either "positive" (paresthesia, dysesthesia, pain) and/or "negative" (hypesthesia, anesthesia) symptoms. The mechanisms underlying these alterations in axonal excitability are not well understood. Clinical tests reveal reduced nerve conduction velocity and axonal loss, but fail to explain nerve excitability. Many different factors have been suggested in relation to the pathophysiology of diabetic neuropathy. There are probably as many factors as there are different clinical pictures in diabetic neuropathy. Nevertheless, it seems that hyperglycemic hypoxia is mainly responsible for the electrophysiological changes seen in damaged diabetic nerves. This article summarizes experimental data indicating that a dysfunction of ion conductances, especially voltage-gated ion channels, could contribute to abnormalities in the generation and/or conduction of action potentials in diabetic neuropathy.

Animals↗
PubMed1981

Experimental allergic neuritis induced by galactocerebroside.

Experimental allergic neuritis (EAN), an animal model of human demyelinative neuritis, was induced by sensitization with galactocerebroside, a glycolipid hapten common in central and peripheral nervous system myelin. Between two months and one year after the initial sensitization, 11 of 24 rabbits immunized repeatedly with bovine brain galactocerebroside (GC) in complete Freund's adjuvant developed a neurological disorder manifested by flaccid quadriparesis, limb hypesthesia, and respiratory paralysis. Seventeen of 20 autopsied rabbits, including all those with clinical illness, had small multiple perivascular foci of demyelinative lesions in roots, dorsal root ganglia, proximal peripheral nerves adjacent to ganglia, and, less frequently, in distal nerves. No change was found in the central nervous system. Demyelination started around venules, with splitting and vesiculation of the outer myelin sheaths of adjacent fibers, and later progressed to form confluent lesions. The lesions were associated with infiltration of phagocytic mononuclear cells, mostly macrophages, which insinuated themselves between myelin lamellae, phagocytized myelin, and subsequently denuded axons. Perivenular infiltration of small lymphocytes, comparable to that seen in whole nerve- induced EAN, was not encountered. The distribution of demyelinative lesions seems to correspond to areas known to have a defective blood-nerve barrier.

Animals↗