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Right hemiparesis with an ipsilateral hypesthesia and ataxia developed in a 57-year-old man. Magnetic resonance imaging showed a left thalamic lacune bordering the medial portion of the posterior limb of the internal capsule. This finding implicated some pathogenetic mechanism of ataxic hemiparesis.
We report a case of essential thrombocythemia, the only clinical manifestation of which consisted of neurologic symptoms, including anomic aphasia, tactile and painful hypesthesia in the right hand, headache, and Gerstmann syndrome, with a relatively benign and slowly progressive clinical course. Neuroradiologic examination disclosed a large ischemic area in the left temporoparietal region. Cerebral angiography revealed an occlusion of the cortical branches of the left middle cerebral artery with total sparing of the carotid vessel. These findings are discussed in relation to the possible pathogenetic mechanisms of the vascular occlusion due to abnormal platelet function in essential thrombocythemia.
There are no published studies evaluating the sensory capacity of the region innervated by the superior laryngeal nerve. A normal sensory capacity is important in this area, since hypesthesia or anesthesia of the pharynx and supraglottic larynx may result in dysphagia and aspiration. This often occurs after stroke or after ablative surgery of the pharynx and larynx. Evaluating the efficacy of restorative procedures for supraglottic and pharyngeal sensation is dependent on defining and quantifying the sensory deficit. We have developed a new, noninvasive method to measure sensation in the pharynx and supraglottic larynx. A puff of air--of precisely controlled duration and pressure--was delivered via a flexible telescope to the anterior wall of the pyriform sinus. Surface sensibility was determined according to the psychophysical method of limits by varying air pressure while holding puff duration constant. We conducted 204 trials in 20 healthy adults. The average sensory discrimination threshold was 2.09 +/- 0.15 mm Hg. An intraclass correlation revealed excellent consistency (R = .80). There was no statistically significant difference between the right and left sides. Brief air pulse stimulation is an easy, relatively safe, and reliable method of determining supraglottic and pharyngeal sensory discrimination thresholds.
Unilateral corneal anesthesia (or hypesthesia) caused by trigeminal nerve disease has an unknown effect on the Schirmer test. Using topical anesthesia, we found that unilateral corneal anesthesia reduces tearing bilaterally, with a greater decrease on the anesthetized side. Clinicians should be aware that trigeminal nerve deficit may alter Schirmer test results, and use bilateral topical corneal anesthesia or alternative methods to stimulate tearing in these cases.
Head and neck manifestations of advanced clival tumors result from subtle, yet progressive mass effect or direct involvement of multiple cranial nerves. Misinterpretation of clinical or radiographic findings in these patients may result in inappropriate treatment planning, increased patient morbidity, and probable tumor recurrence. Our combined experience in managing 21 patients with advanced clival tumors has shown that preoperative loss of vision, diplopia, or facial hypesthesia suggests superior parasellar disease. Facial twitching or neurotologic symptoms result from posterior central tumor growth, while inferior extension of disease leads to basal cranial nerve deficits with associated speech, voice, and swallowing dysfunctions. The purpose of this article is to correlate the complex anatomy of the clivus, brainstem, and cranial base and the various neurotologic findings associated with neoplasms in this region. Lateral skull base surgical procedures, based on preoperative clinicoradiographic assessment, will be detailed with particular emphasis on preservation of critical neurovascular structures.
Twenty-six patients (30 hands) who underwent endoscopic carpal tunnel release were physically examined and asked to complete questionnaires on their symptoms, functional limitations and satisfaction. Their mean grip strength improved considerably from 17.5 kg before the operation to 31.3 kg at the final follow-up. Symptoms at the final follow-up were hypesthesia in 9 hands, muscle atrophy in 10, positive Tinel sign in 3, and positive Phalen sign in 1. The mean symptom severity score improved from 3.01 before the operation to 1.44 at the final follow-up and the mean functional status score improved from 3.20 to 1.54. The average times to return to activities of daily living and work were 7.3 days and 18.4 days respectively. Twenty-two of the 26 patients (85%) were satisfied. There was no injury to neurovascular structures. Arterial injuries were prevented by marking the superficial palmar arch and ulnar artery with a Doppler ultrasonic hemodrometer before surgery.
Notalgia paresthetica was described by Astwazaturow in 1934. We have seen six cases in the past year, suggesting that it is not rare. This sensory neuritis affects the posterior rami of several spinal nerves (arising from thoracic segments T2 to T6), causing pruritus, burning, and dysesthesias. Examination reveals hypesthesia. Although the cause is not known, the course seems benign. The posterior rami of these five dorsal roots traverse a 90-degree course through the multifidus spinae muscle, making them unique among the posterior rami.
The prevalence of peripheral neuropathy in 186 epileptic patients was 16.7%. The neuropathy was characterized by stocking hypesthesia and reduced Achilles reflexes, and it occurred with all anticonvulsant agents. Electrophysiologic tests indicated slowing of peroneal and sural nerve conduction velocity and prolongation or absence of H reflexes and F responses. The prevalence of neuropathy was not greater in patients receiving phenytoin, and there was no relationship between clinical or electrical abnormalities and blood levels or duration of treatment for either phenytoin or phenobarbital. We did not find a specific relationship between phenytoin usage and peripheral neuropathy in epileptic patients.
Three patients with skin cancer had numbness isolated to one cheek, in the distribution of the infraorbital nerve. Hypesthesia also involved the medial and lateral upper incisors and canine teeth, and adjacent gingiva, sparing the more posterior teeth and gums. The molar and premolar teeth and gums are innervated by the posterior and middle superior alveolar nerves; because these structures were spared, the pathologic process was localized to the infraorbital foramen, and we could exclude involvement of the maxillary division more proximally. In two patients, cheek numbness heralded recurrent squamous cell carcinoma. Analogous anatomy at the mental foramen should help distinguish intracranial leptomeningeal from local mandibular lesions producing isolated numbness of the chin.
We studied a 33-year-old woman with a negative family history. Both of her parents were examined clinically by nerve conduction velocities (NCVs) and EMG, with normal results. The clinical onset of her condition was at 24 months, with severe weakness and atrophy of her feet and hands, but the proximal muscles were relatively spared. She had bilateral pes cavus, distal weakness and hypesthesia for touch and proprioception, areflexia, claw hands, and severe thoracolumbar kyphoscoliosis. NCVs showed absent motor and sensory responses and EMG revealed diffuse fibrillation potentials. Molecular genetic studies indicated a de novo dominant missense point mutation of exon 3 of the peripheral myelin protein 22 gene at nucleotide 264 that caused the replacement of serine with leucine.
We studied two families with X-linked dominant Charcot-Marie-Tooth neuropathy. The clinical findings included onset around age 14 years, with moderate weakness of feet extensors and palmar and dorsal interossei, areflexia, distal hypesthesia, and slow progressivity. Motor nerve conduction velocities showed slowing (20 to 30 m/sec) and EMGs were normal. Genetic linkage analysis revealed positive lod scores with the markers of the Xq13.1 region in family 2, but was noninformative in family 1. There were no point mutations in the connexin32 gene coding region. Instead, family 1 revealed a T-to-G transversion at position -528 relative to the ATG start codon, whereas family 2 showed a C-to-T transition at position -458. The first mutation is located in the nerve-specific connexin32 promoter just upstream of the transcription start site, the second is located in the 5' untranslated region of the mRNA.
UNLABELLED: We compared the central nervous system (CNS) and cardiovascular effects of levobupivacaine and ropivacaine when given IV to healthy male volunteers (n = 14) in a double-blinded, randomized, crossover trial. Subjects received levobupivacaine 0.5% or ropivacaine 0.5% after a test infusion with lidocaine to become familiar with the early signs of CNS effects (e.g., tinnitus, circumoral paresthesia, hypesthesia). The development of CNS symptoms was assessed at 1-min intervals and study drug administration was terminated when the first CNS symptoms were recognized. Thereafter, symptoms were recorded at 1-min intervals until symptom resolution. Hemodynamic variables were assessed by transthoracic electrical bioimpedance. Continuous 12-lead electrocardiogram monitoring was also performed. There was no significant difference between levobupivacaine and ropivacaine for: the mean time to the first onset of CNS symptoms (P = 0.870), mean total volume of study drug administered at the onset of the first CNS symptom (P = 0.595), stroke index (P = 0.678), cardiac index (P = 0.488), acceleration index (P = 0.697), PR interval (P = 0.213), QRS duration (P = 0.637), QT interval (P = 0.724), QTc interval (P = 0.737), and heart rate (P = 0.267). Overall, fewer CNS symptoms were reported for levobupivacaine than ropivacaine (218 versus 277). This study found that levobupivacaine and ropivacaine produce similar CNS and cardiovascular effects when infused IV at equal concentrations, milligram doses, and infusion rates. IMPLICATIONS: This study compared directly, for the first time, the toxicity of levobupivacaine and ropivacaine in healthy volunteers. Levobupivacaine and ropivacaine produced similar central nervous system and cardiovascular effects when infused IV at equal concentrations, milligram doses, and infusion rates.
We determined the incidence, distribution, and resolution of neurologic sequelae and the association with anesthetic, surgical, and patient factors after single-injection interscalene block (ISB) using levobupivacaine 0.625% with epinephrine 1:200,000 in subjects undergoing shoulder or upper arm surgery, or both, in 693 consecutive adult patients. After a standardized ISB, assessments were made at 24 and 48 h and at 2 and 4 wk for anesthesia, hypesthesia, paresthesias, pain/dysesthesias, and motor weakness. Symptomatic patients were monitored until resolution. Subjects reporting pain or discomfort >3 of 10 and those with motor or extending sensory symptoms received diagnostic assessment. Six-hundred-sixty subjects completed 4 wk of follow-up. Fifty-eight neurologic sequelae were reported by 56 subjects. Symptoms were sensory except for two cases of motor weakness (lesions identified distant from the ISB site). Thirty-one sequelae with likely ISB association were reported by 29 subjects, including 14 at the ISB site, 9 at the distal phalanx of thumb/index finger, 7 involving the posterior auricular nerve, and 1 clinical brachial plexopathy. Sequelae not likely associated with the ISB were reported by 27 subjects with symptoms reported in the median (n = 9) and ulnar (n = 4) nerves, surgical neuropraxias (n = 12), and motor weakness (n = 2). Symptoms resolved spontaneously (median 4 wk; range, 2-16 wk) except in the two patients with motor weaknesses and the patient with clinical brachial plexopathy, who received therapeutic interventions. Variables identified as independent predictors of neurologic sequelae likely related to ISB were paresthesia at needle insertion and ISB site pain or bruising at 24 h. In contrast, surgery preformed in the sitting position, as well as ISB site bruising, was identified as a predictor of neurologic sequelae not likely related to ISB. In conclusion, neurologic sequelae after single-injection ISB using epinephrine mainly involve transient minor sensory symptoms.
Seventy-six patients underwent the primary removal of an acoustic neurinoma at the Mayo Clinic from 1978 through 1980. Hearing loss was present in 97% of the patients, and tinnitus and dysequilibrium occurred in 70% of the patients. The most common signs were a decreased corneal reflex, nystagmus, and facial hypesthesia. In these patients, pure tone and speech audiometry are used to define the hearing loss. When hearing is still present, the speech discrimination is often disproportionately low. Acoustic reflex testing and brain stem evoked response are used to determine whether the hearing loss is cochlear or retrocochlear. When these tests could be performed in this series of patients, they were accurate in 85 to 95%. The vestibular response to caloric testing is expected to be decreased or absent in about 90% of patients, and this was so in 86% of our patients. Radiographic studies are the most important tests currently used for the diagnosis of acoustic neurinoma. Tomography of the internal auditory canal shows abnormalities in 80% of patients. Computed tomography with contrast enhancement demonstrates abnormalities in 90% of patients. The computed tomographic (CT) scan may reveal the location, the size, and often the consistency of the tumor. In cases still questionable after CT scanning, positive contrast rhombencephalography is used for clarification. In this series, no single symptom, sign, abnormal audiometric test result, or abnormal radiographic finding was present in all patients; therefore, the most important factor in diagnosis is an alert physician.
Fourteen patients with acoustic neurinomas varying in size from 7 to 30 mm were treated by stereotactic radiosurgery and then were followed for 4 years. The tumors of eight patients decreased 1 to 10 mm in diameter, no change was found in two, and the tumor increased slightly in three patients. Loss of the ability to enhance with contrast administration on computed tomographic scan was a common effect of the treatment. One patient in poor general condition died from intercurrent disease 6 months after radiosurgery. At postmortem examination, a large central necrosis was found. Among five patients with hearing before treatment, full preservation was demonstrated in one; in the other four, the mean impairment of speech discrimination score was 43%. One patient with total unilateral deafness regained hearing and achieved a discrimination score of 60% at 1 year after treatment. There was transient facial weakness in five patients, which was detectable only by electromyography in one. Facial hypesthesia appeared in two patients and was transitory in one of them. Thirteen of the patients are in good or excellent general condition. Stereotactic radiosurgery offers the only therapeutic alternative to open operation in the management of acoustic neurinomas. It is worth considering for every patient, but especially for poor risk patients and those with bilateral tumors.
OBJECTIVE AND IMPORTANCE: Paragangliomas of the thoracic spine are rare. Previously described cases involved nonfunctioning tumors. This report documents the diagnosis and surgical treatment for a patient who presented with a functioning thoracic paraganglioma. CLINICAL PRESENTATION: A 53-year-old woman presented with a 10-month history of headaches, facial flushing, and palpitations associated with hypertension. Urinary catecholamine levels were markedly elevated. Magnetic resonance imaging and m-[(123)I]iodobenzylguanidine scans demonstrated an extradural tumor located within the T12 vertebra, with a significant paraspinal component. The neurological examination revealed mild hypesthesia in the right T12 dermatome. INTERVENTION: The patient underwent resection of the tumor after alpha-adrenergic receptor blockade. Grossly complete excision was achieved without neurological complications. Postoperatively, the patient was normotensive and exhibited catecholamine levels within the normal range. CONCLUSION: Functioning paragangliomas of the thoracic spine are rare lesions that are difficult to treat. Successful treatment requires careful surgical planning and expert pharmacological manipulation.
A review of the otoneurologic findings in 500 patients with facial paralysis revealed their importance for diagnosis, prognosis, and understanding the pathophysiology of Bell's palsy. Diagnosis. The presence of simultaneous bilateral palsy, facial paralysis associated with lateral rectus palsy, slowly progressive facial weakness with or without hyperkinesis, and facial paralysis that showed no recovery after six months excluded Bell's palsy from the diagnosis. Ipsilateral recurrent palsies were another indication to suspect an underlying cause, since a tumor of the facial nerve caused the paralysis in 30% of the patients with this finding. Signs such as intact forehead movement, alterations in facial sensation, and corneal hypesthesia--although often associated with lesions in the cerebral cortex, cerebellopontine angle, or internal auditory canal--were also found in patients with Bell's palsy. Prognosis. A spontaneous complete recovery following Bell's palsy occurs in about 70% of the patients; but in the presence of a dry eye or dysacousis, the prognosis for a complete recovery drops 10 and 25%, respectively. Pathophysiology. It is proposed that the wide range of neurologic findings associated with Bell's palsy is due to a viral polyneuropathy. This is a disorder that primarily involves sensory nerves, and the facial motor deficit results from involvement of the sensory fibers carried with the facial nerve within the fallopian canal.
Dysthyroid exophthalmopathy (orbitopathy) results from an enlargement of extraglobal orbital structures, producing ocular proptosis, optic nerve compression, and corneal exposure. Treatment with corticosteroids and radiation may be beneficial; refractory cases require surgical decompression of the orbit. Transantral orbital decompression was described by Walsh and Ogura and has been performed in over 350 patients at this institution. A review of 305 patients with long-term follow-up was performed. Visual acuity improved or was maintained at preoperative levels in over 95% of the patients, with ocular recession ranging from 1 to 12 mm (average: 4 mm). Postoperative ocular balance of relative exophthalmos was to within 1 mm in 76% of the patients and to within 2 mm in approximately 90% of the patients. Normal postoperative extraocular muscle balance was present in 99 patients. Immediate postoperative diplopia was noted in 206 patients. Long-term follow-up revealed that in 137 of these patients, diplopia resolved or responded to conservative management. Extraocular muscle surgery was required for correction in 69 patients. Twenty-seven patients had postoperative complications. These included 16 patients with hypesthesia of the infraorbital nerve, 5 patients with sinusitis, 3 patients who had incomplete decompression, 2 patients with oral antral fistulae, and 1 patient who had CSF rhinorrhea. Five patients, despite surgery, radiation, and steroid therapy progressed to blindness. We conclude that this procedure is effective and carries few complications. Orbital imaging, using computed tomography or magnetic resonance sequence with reconstructive capabilities, permits early diagnosis and treatment of dysthyroid compression optic neuropathy.