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

Although swallowing difficulties (dysphagia) frequently occur in acute brainstem infarction, physiological studies of dysphagia (videofluoroscopy, manometry) are rarely reported. We present a patient with ipsilateral Horner's syndrome, palatal and laryngeal weakness, aphagia, and ipsilateral face and contralateral extremity pin and temperature loss due to lateral medullary infarction confined to the rostral dorsolateral medulla (RDM). Videofluoroscopy showed that the patient was unable to initiate a swallow. Manometry showed a markedly reduced peak pharyngeal pressure and weak pharyngeal contractions. Within 20 months, the patient's neurological deficits resolved, videofluoroscopy showed a normal swallow, and manometry showed normal peak pharyngeal pressure. Correlation of the clinical, physiological, and imaging evaluations shows that aphagia and severe bilateral pharyngeal paresis can result from unilateral RDM infarction. We suggest that, in man, the bilateral medullary swallowing centers function as one integrated center, and that infarction of a portion of this center is sufficient to cause complete loss of swallowing.
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PMID:Aphagia due to pharyngeal constrictor paresis from acute lateral medullary infarction. 956 69

We report a 75-year-old hypertensive man presented with unilateral MLF syndrome combined with ipsilateral blepharoptosis and trochlear nerve paresis due to midbrain infarction. He was admitted to our hospital for sudden onset of diplopia. Neurological examination revealed left ptosis, infraduction disorder of the left eye and left MLF syndrome. Horner's syndrome or other focal neurological signs were not observed; convergence was preserved. Hess-charts confirmed left superior oblique paresis and left internuclear ophthalmoplegia. Laboratory data were all normal. T2-weighted images of brain MRIs demonstrated a high-signal intensity lesion in the paramedian dorsal midbrain at the inferior colliculus level, anterior to the cerebral aqueduct. The oculomotor dysfunction and diplopia had disappeared at discharge, although slight ptosis persisted. It is likely that the lesion in our case affected the left MLF, the right trochlear nucleus or its fascicles and the left partial oculomotor fascicles. Cases with MLF syndrome associated with trochlear nerve palsy have been rarely reported. Our case suggests that the fibers controlling for the musculus levator palpebrae superioris are located more caudally in the oculomotor fascicles.
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PMID:[Midbrain infarction presenting with unilateral blepharoptosis, trochlear nerve paresis and MLF syndrome]. 986 19

Four newborn boys developed respiratory insufficiency and pneumothorax, pneumomediastinum or subcutaneous emphysema as the result of a laryngeal or tracheal rupture. These ruptures were due to birth injuries after difficult labour resulting from shoulder dystocia or a large lymphangioma and to a birth weight of at least 4500 g. The three children with shoulder dystocia also had a clavicular fracture, a Horner's syndrome, Erb paralysis or phrenic nerve paresis. Treatment consisted of surgical repair followed by a few days' intubation. The children with a shoulder dystocia recovered well, although in one of them a tracheal stenosis had to be resected a few months later. The child with the lymphangioma died from a bifurcation embolus. In newborns with respiratory insufficiency and pneumomediastinum or subcutaneous emphysema after a difficult delivery an emergency laryngotracheoscopy has to be performed to exclude rupture of larynx or trachea.
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PMID:[Rupture of larynx or trachea resulting from injuries sustained at birth]. 1044 82

The course and distribution of the facial corticobulbar tract (CBT) was examined by correlating MRI of brain stem lesions with neurological symptoms and signs including central (C-FP) or peripheral facial paresis (P-FP) in 70 patients with localised infarction of the lower brain stem. C-FP occurred more often in patients with lesions of the lower pons or upper medulla of the ventromedial brain stem. Some patients with dorsolateral infarcts of the upper medulla to the lower pons showed C-FP, mostly on the lesion side. P-FP on the side of the lesion was also seen in patients with dorsolateral involvement of the lower pons. Patients with ventromedial infarction of the brain stem showed paresis of extremities contralateral to the lesion. Specific neurological symptoms and signs such as dysphagia, vertigo, nystagmus, Horner's syndrome, ipsilateral cerebellar ataxia, and contralateral superficial sensory impairment were seen in patients with dorsolateral infarcts of the brain stem. It is hypothesised that the facial CBT descends at the ventromedial lower pons, near the corticospinal tract, mainly to the level of the upper medulla, where the fibres then decussate and ascend in the dorsolateral medulla to synapse in the contralateral facial nucleus.
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PMID:Course and distribution of facial corticobulbar tract fibres in the lower brain stem. 1089 7

We report a 51-year-old man with mild left central facial palsy and left Avellis' syndrome due to a small medullary infarction. On admission, neurological examination revealed hoarseness, dysphasia, absent left gag reflex, palsies of the left vocal cord and left soft palate, and hypalgesia and thermohypesthesia on the right side of the trunk and extremities. In addition, he had a mild left central facial palsy. He had no nausea, vomiting, vertigo, hiccups, nystagmus, Horner's sign, facial numbness, or paresis or ataxia of the limbs. A T2 weighted MRI showed a small, high signal intensity area in the left dorsal region of the medulla and this lesion was presumed to involve the nucleus ambiguus and a part of the spinothalamic tract. These findings suggest that an aberrant supranuclear pathway, looping around the nucleus ambiguus to the facial nucleus exists in our patient.
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PMID:[A case of Avellis' syndrome with ipsilateral central facial palsy due to a small medullary infarction]. 1096 64

A young adult male white Bengal tiger (Panthera tigris tigris) presented with hindlimb ataxia. Cervical and lumbar myelography revealed a compressive lesion of the cord at C(6-7). Corticosteroid therapy and confinement failed to provide lasting remission of signs. A modified, inverted cone ventral slot decompression was used to remove the fibrous material causing cord compression at C(6-7). Temporary Horner's syndrome and laryngeal paresis developed postsurgically because of excessive tissue retraction. The animal recovered normal ambulatory function 6 wk after surgery.
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PMID:Caudal cervical disc protrusion in a Bengal tiger (Panthera tigris tigris). 1123 51

Cranial nerve palsy in internal carotid artery (ICA) dissection occurs in 3--12% of all patients, but in 3% of these a syndrome of hemicranias and ipsilateral cranial nerve palsy is the sole manifestation of ICA dissection, and in 0.5% of cases there is only cranial nerve palsy without headache. We present two cases of lower cranial nerve palsy. The first patient, a 49-year-old woman, developed left eleventh and twelfth cranial nerve palsies and ipsilateral neck pain. The angio-RM showed an ICA dissection with stenosis of 50%, beginning about 2 cm before the carotid channel. The patient was treated with oral anticoagulant therapy and gradually improved, until complete clinical recovery. The second patient, a 38-year-old woman, presented right hemiparesis and neck pain. The left ICA dissection, beginning 2 cm distal to the bulb, was shown by ultrasound scanning of the carotid and confirmed by MR angiogram and angiography with lumen stenosis of 90%. Following hospitalisation, 20 days from the onset of symptoms, paresis of the left trapezius and sternocleidomastoideus muscles became evident. The patient was treated with oral anticoagulant therapy and only a slight right arm paresis was present at 10 months follow-up. Cranial nerve palsy is not rare in ICA dissection, and the lower cranial nerve palsies in various combinations constitute the main syndrome, but in most cases these are present with the motor or sensory deficit due to cerebral ischemia, along with headache or Horner's syndrome. In the diagnosis of the first case, there was further difficulty because the cranial nerve palsy was isolated without hemiparesis, and the second case presented a rare association of hemiparesis and palsy of the eleventh cranial nerve alone. Compression or stretching of the nerve by the expanded artery may explain the palsies, but an alternative cause is also possible, namely the interruption of the nutrient vessels supplying the nerve, which in our patients is more likely.
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PMID:Spontaneous carotid dissection presenting lower cranial nerve palsies. 1123 57

A 17-year-old male presented with a wound on the right temporal region, oozing hemorrhagic necrotic brain tissue and cerebrospinal fluid, following a fall. Computed tomography showed temporoparietal and petrous apex fractures on the right. Neurological examination revealed abducens nerve paresis, ptosis, and myosis on the right side. The patient was treated surgically for the removal of the free bony fragments at the fracture site and to close the dural tear. The abducens nerve paresis, ptosis, and myosis persisted at the 3rd monthly postoperative follow-up examination. The anatomy of the abducens nerve at the petroclival region was studied in four cadaveric heads. Two silicone-injected heads were used for microsurgical dissections and two for histological sections. The abducens nerve has three different angulations in the petroclival region, located at the dural entrance porus, the petrous apex, and the lateral wall of the cavernous segment of the internal carotid artery. The abducens nerve had fine anastomoses with the trigeminal nerve and the periarterial sympathetic plexus. There were fibrous connections extending inside the venous space of the petroclival area. The abducens nerve seems to be vulnerable to damage in the petroclival region, either directly by trauma to its dural porus and petrous apex or indirectly by stretching of the nerve through the nervous and/or fibrous connections. Concurrent functional loss of the abducens nerve and the periarterial sympathetic plexus clinically manifested as incomplete Horner's syndrome in our patient.
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PMID:Isolated abducens nerve paresis associated with incomplete Horner's syndrome caused by petrous apex fracture--case report and anatomical study. 1176 Mar 84

The medical records of 29 dogs unable to close their mouths due to flaccid paralysis or paresis of the muscles innervated by the mandibular branch of the trigeminal nerve, were reviewed. Idiopathic trigeminal neuropathy was diagnosed in 26 dogs based on complete resolution of clinical signs and lack of any long-term neurological disease. Of these dogs, golden retrievers were overrepresented. No age, sex, or seasonal predispositions were identified. Trigeminal sensory innervation deficits were observed in 35% (9/26), facial nerve deficits were observed in 8% (2/26), and Horner's syndrome was observed in 8% (2/26) of dogs. Electromyographic examination of the muscles of mastication revealed abnormalities in seven of nine dogs. Results of cerebrospinal fluid analysis were abnormal in seven of eight dogs. Corticosteroid therapy did not affect the clinical course of the disease. Mean time to recovery was 22 days. Lymphosarcoma, Neospora caninum infection, and severe polyneuritis of unknown origin were diagnosed in three of 29 dogs at necropsy.
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PMID:Trigeminal neuropathy in dogs: a retrospective study of 29 cases (1991-2000). 1202 13

An increasing number of complications are being noted with the widespread use of oral contraceptives (OCs). In opthalmology, migraine like headaches are frequently encountered. This report presents observations of 4 different neurological manifestations in 4 different individuals in addition to the headache for which they were referred to the Neuro-Ophthalmology Clinic of the Philippine General Hospital. The 4 cases clearly demonstrate that aside from the headache neuro ophthalmologic abnormalities can occur during OC use: left facial paresis, left Horner's syndrome, bilateral ptosis, and left mydriasis. The abnormalities disappeared on withdrawal of the OCs, suggesting that they are caused by the drug. They were reversible after 2 months to 4 years of medication. OCs are combinations of semisynthetic progesterone and estrogen. A study of 2 of the cases suggests that the estrogen portion may be the responsible agent for these pathologies. They did not reappear with the intake of another OC containing a lower concentration of ethinyl estradiol (.035 mg instead of .05 mg). This may present some problems in family planning for it is recommended that at least .05 mg of estrogen be incorporated with progesterone in order to have the pill most effective as a contraceptive agent. Examination of the neurologic complications encountered in these 4 patients suggests that intracerebral vascular deficiency has occurred simulating isolated small arterial occlusions.
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PMID:Neuro-ophthalmological complications of contraceptive pills. 1233 85


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