Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of epidermoid tumor of the lateral ventricle. Epidermoid tumors are relatively uncommon intracranial lesions and the one situated in the lateral ventricle has not been reported in this country. A 42 year old house wife was admitted to Asahi Central Hospital on February 14, 1973, complaining of progressive right hemiparesis for 2 years. The patient had no headache and no other symptoms of increased intracranial pressure. Neurological examination revealed disorientation, dyscalculia, amnestic aphasia, morter dysphasia, right facial paresis (central type) and right hemiparesis. The laboratory findings, which included complete blood count, serum electrolytes, urinalysis, electrocardiogram and blood Wassermann, were normal. Initial pressure of the spinal tap was 410 mmH2O and crystal clear CSF was obtained. tplain craniogram showed no calcification and was normal. The left CAG showed clearly the signs of the temporal lobe tumor (Fig. 1, 2, 3, 4.), but showed no early veins and no tumor stains. The brain scintigram was normal. A left temporo-parietooccipital craniotomy was performed. The epidural Echogram (horizontal section-Fig. 5, coronall section-Fig. 6) revealed the clear demarcated, multicystic round tumor in the inferior horn of the left lateral ventricle. After the whitesoap like tumor was totaly removed, the all interior surface of the left inferior horn of the lateral ventricle was seen (Fig. 8). Tumor was 5.5 cm in diameter and 50 g in weight. Histological findings of the tumor showed typical epidermoid (Fig. 9, 10). The origin of the intravetricular epidermoids and the usefulness of echo-encephalorgaphy were briefly discussed.
 ...
PMID:[The epidermoid tumor of the lateral cerebral ventricle; report of a case (author's transl)]. 94 14

An 8-year-old nongravid female llama with a 1-month history of progressive posterior paresis was referred because of suspected degenerative myelopathy secondary to copper deficiency or plant poisoning. Neurologic examination revealed loss of conscious proprioception and slightly depressed bilateral patellar reflexes. Electromyographic examination of hindlimb flexors and extensors did not elicit evidence of lower motor neuron disease. Possible fragmentation and mottling of the 10th thoracic vertebral body were noted radiographically. Results of a lumbar CSF tap, complete blood count, and fecal flotation were not diagnostic. In the face of poor prognosis, the llama was euthanatized. Postmortem and histologic evaluation revealed, in addition to disseminated visceral granulomas, an extradural pyogranulomatous mass compressing the cord laterally at the level of T-10. Large numbers of Coccidioides immitis were dispersed throughout the granulomas. Complement fixing antibody tests in 11 other herd members showed evidence of C immitis infection in three.
 ...
PMID:Coccidioidomycosis in the llama: case report and epidemiologic survey. 717 54

Although ocular manifestations of Lyme disease have long been noted, they remain a rare feature of the disease. The spirochete invades the eye early and remains dormant, accounting for both early and late ocular manifestations. A nonspecific follicular conjunctivitis occurs in approximately 10% of patients with early Lyme disease. Keratitis occurs often within a few months of onset of disease and is characterized by nummular nonstaining opacities. Inflammatory syndromes, such as vitritis and uveitis, have been reported; in some cases, a vitreous tap is required for diagnosis. Neuro-ophthalmic manifestations include neuroretinitis, involvement of multiple cranial nerves, optic atrophy, and disc edema. Seventh nerve paresis can lead to neurotrophic keratitis. In endemic areas, Lyme disease may be responsible for approximately 25% of new-onset Bell's palsy. Criteria for establishing that eye findings can be attributed to Lyme disease include the lack of evidence of other disease, other clinical findings consistent with Lyme disease, occurrence in patients living in an endemic area, positive serology, and, in most cases, response to treatment. Management of ocular manifestations often requires intravenous therapy.
 ...
PMID:Ocular manifestations of Lyme disease. 772 93

We report a 55-year-old man with papilledema and multiple cranial nerve palsies. He was well until 52 years of age when there was an onset of progressive difficulty in initiating urination; he visited the urology service of our hospital where a diagnosis of prostate cancer was made; the cancer was invading the bladder and was metastasizing to lymph nodes and bones. He was treated with oochiectomy and estrogen preparations with some improvement in his symptoms. Two years later, he developed difficulty in urination again, and transurethral resection of the tumor was performed in 1991. In December 1991, he noted tingling and numb sensation in his left face, which had become progressive worse within the next one month, and he developed blepharoptosis and deafness all on the left side. He was admitted to the urology service on February 4, 1992, and a neurological consultation was asked. On physical examination, general findings were unremarkable, except for lymph node enlargements of about 0.5 to 1.0 mm in size in cervical and inguinal regions. On neurologic examination, he was alert with normal mental activities; higher cerebral functions were intact. He had normal vision and visual fields, however, papilledema was present bilaterally; pupils and light reactions were normal. Extraocular muscles were intact on the right side, however, moderate restriction was noted in the left eye in that all the extraocular muscles except for the medial rectus were weak; blepharoptosis was noted on the left; no nystagmus was present. The sensation was diminished in the left face, and left facial paresis of the peripheral type was also noted; the taste sensation was also diminished in the left anterior two thirds of the tongue. He had sensorineural deafness on the left side. The other cranial nerves appeared intact. He walked normally; no weakness or muscle atrophy was noted; muscle tone was normal and no ataxia was observed. Deep reflexes were normally elicited and symmetric; the plantar response was flexor. No meningeal signs were present. Laboratory examination revealed following abnormalities: Hb 7.1 g/dl, platelet 47,000/cmm, WBC3,800/cmm, LDH 950IU/l, PAP232ng/ml (normal less than 1.6), PA2.631ng/ml (normal less than 7.4); a small amount of effusion was noted in the left pleural cavity; cytological examination of the fluid was class V. A cranial CT scan as well as MRI were entirely normal, as was the spinal tap. He was treated with glycerol, however, there was progressive increase in the pleural effusion, and he developed dyspnea; moist rale had become audible in the end of February.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[A 55-year-old man with prostate cancer, papilledema, and multiple cranial nerve palsies]. 794 37

Since the first paraplegic centre was established in 1945, life expectancy and life quality of paraplegics have considerably improved. However, endeavours to enhance the mobility of these patients have been less successful. The most promising approach, functional electric stimulation of paralysed muscles, is poorly accepted by patients at present because of technical problems. This study describes current approaches which may help to improve patients' mobility. A central motor lesion is perceived by the patient as a movement disorder of the legs, e.g. a gait disorder. Neurological investigation indicates, on the basis of exaggerated tendon reflexes and increased resistance of the non-activated leg muscles to stretching, that spastic paresis underlies the movement disorder. This combination of symptoms and clinical (physical) signs suggests that the exaggerated tendon tap reflexes are responsible for muscle hypertonia and the latter causes the movement disorder. However, electromyography during movement shows that the exaggerated short latency reflexes are associated with loss or attenuation of the functionally essential polysynaptic spinal reflexes. In the event of impaired supraspinal control there is loss of monosynaptic stretch reflex inhibition combined with reduced facilitation of polysynaptic spinal reflexes. Development of tension in tonically active calf muscles in patients with spastic paresis during gait occurs independently of spinal reflex activity. From electrophysiological and histological observations it can be assumed that transformation of motor units resulting in simple and less well adapted regulation of muscle tone allows movements such as gait. The reduction of muscle tone obtained with antispastic drugs is usually associated with paresis and may therefore hamper locomotion. Locomotor training represents a new attempt to improve the mobility of patients with incomplete paraplegia. It includes activation of neuronal circuits within the spinal cord below the level of the lesion. In incomplete paraplegics a coordinated leg muscle activation pattern and corresponding leg movements can be triggered and trained in patients standing on a treadmill with partial weight support. Improvement of training of the spinal cord locomotor centre can be expected from triggering of spinal cord reflexes and regeneration of spinal tract fibres, which is expected to be possible in the near future.
 ...
PMID:[Focus on current research: improving the mobility of paraplegic patients]. 1089 54

An acute central nervous system lesion is followed by a phase of "shock" with flaccid muscle tone. After some weeks the syndrome of spastic paresis develops which is characterized by increased muscle tone and exaggerated tendon tap reflexes. During the last years it could be shown that the characteristic spastic movement disorder is mainly due to secondary changes of muscle properties which require a specific treatment. Exaggerated reflexes do only little contribute to the movement disorder.
 ...
PMID:[Basic principles and therapy of spasticity]. 1114 82

Caloric testing of the vestibular labyrinth is usually performed by classical caloric test procedures (CCTP) using water warmed to 30 degrees C and 44 degrees C. Ice water irrigation (4 degrees C) is usually not performed, although it might be useful as a bedside test. To verify the validity of the Minimal Ice Water Caloric Test (MIWCT), comparative video-oculographic investigations were performed in 22 healthy subjects using ice water (0.5 ml, 1.0 ml, 2 ml), CCTP, and cold air (27 degrees C). Frequency, amplitude, slow phase velocity (SPV), the onset, and the duration of nystagmus were documented. After addition of three ice cubes, the temperature of conventional tap water (16 degrees C) fell within 13 min to 4 degrees C. In pessimum position the subjects demonstrated no nystagmus response. Compared to CCTP, MIWCT was associated with a significantly later onset of nystagmus and a significant prolongation of the nystagmus reaction. In contrast to air stimulation (27 degrees C), a significant Spearman's correlation was noted between MIWCT (1 and 2 ml) and established CCTP in respect of essential nystagmus parameters (frequency, amplitude and SPV). Furthermore, MIWCT (0.5 and 1 ml) showed a higher sensitivity and specificity with regard to the detection of canal paresis based on Jongkees' formula compared to stimulation with air 27 degrees C. Thus, MIWCT appears to be a suitable procedure for bedside investigation of vestibular function outside the vestibular laboratory, e.g. in a hospital ward, where bedridden patients with vertigo occasionally require vestibular testing.
 ...
PMID:The minimal ice water caloric test compared with established vestibular caloric test procedures. 1628 3

In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are generally thought to be responsible for spastic movement disorders. Most antispastic treatments are, therefore, directed at the reduction of reflex activity. In recent years, however, researchers have noticed a discrepancy between spasticity as measured in the clinic and functional spastic movement disorders, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behaviour of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fibre, collagen tissue, and tendon properties (eg, loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organisation. Antispastic drugs can accentuate paresis and therefore should be applied with caution in mobile patients.
 ...
PMID:Spastic movement disorder: impaired reflex function and altered muscle mechanics. 2922 72

Antispastic medications that are directed to reduce clinical signs of spasticity, such as exaggerated reflexes and muscle tone, do not improve the movement disorder. Medication can even increase weakness which might interfere with functional movements, such as walking. In this chapter we address how spasticity affects mobility and how this should be taken into account in the treatment of spasticity. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are the consequence of spinal cord injury (SCI). They are generally thought to be responsible for spastic movement disorders. Most antispastic treatments are, therefore, directed at the reduction of reflex activity. In recent years, a discrepancy between spasticity as measured in the clinic and functional spastic movement disorder was noticed, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behavior of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fiber, collagen tissue, and tendon properties (e.g., loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organization. Antispastic drugs should primarily be applied in complete SCI. In mobile patients they can accentuate paresis and therefore should be applied with caution.
 ...
PMID:Spasticity. 2309 14

Ventriculoperitoneal (VP) shunt surgery is probably the commonest surgical procedure in neurosurgery. Belying its technical simplicity is the myriad complications associated with it. Shunt malfunction is a common complication associated with this surgery, second only to shunt related infections, which may be associated with it. Sterile cerebrospinal fluid (CSF) eosinophilia (CE) has been reported with VP shunts, which may or may not be related to the dysfunction. Eosinophilia in the CSF has also been associated with a number of other conditions including parasitic infestations in the brain. This may be unrelated to the shunt surgery. We present a case of a child, operated earlier for hydrocephalus, who presented with sub-acute loss of vision and bilateral oculomotor paresis. CSF from a chamber tap revealed eosinophilia. The commonest presenting symptom of shunt malfunction is raised intracranial pressure. There are no reports in the literature of VP shunt malfunction presenting with bilateral oculomotor paresis and decreased visual acuity. The associated CE complicated the clinical picture, especially since the initial brain radiology was normal. We discuss the clinical differential diagnosis of this very interesting presentation, management dilemmas and outcome in this child. This rare clinical presentation was found to be the result of a shunt malfunction and not due to any rare parasitic infestation of the brain. Occam's razor dictates that the simplest explanation in a given situation is usually the most accurate, as is seen in this case.
...
PMID:Occam's razor in the management of ventriculoperitoneal shunt dysfunction: Diagnosis and management of an unusual pediatric case. 2597 62


1