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At least 793 records · Page 44Linked to original sources
PubMed1999

Follow-up findings in regional cerebral blood flow (r-CBF)-SPECT in a case of idiopathic childhood hemidystonia. Functional neuroimaging and pathophysiological implications.

A 9 1/2-year-old girl suffered from intermitting tremor and jitteriness of her left hand and oral muscles every 4 to 6 weeks with long lasting episodes. Clinically myoclonias and dystonic positioning of the left arm, hand and facial muscles were seen. No evidence of trauma, infection or inborn errors of metabolism was found. Successful therapy with carbamazepine was initiated while L-DOPA failed. An ictal 99m-Tc-HMPAO-SPECT showed severe asymmetry with focal hyperperfusion of the contralateral right thalamus and basal ganglia as well as of the bifrontal cortex, whereas no anatomical lesions were found by MRI. In contrast, an interictally performed 99m-Tc-HMPAO SPECT showed hypoperfusion of the right thalamus and normalisation of the frontal perfusion under medical treatment. These 99m-Tc-HMPAO-SPECT findings may provide new insights into the localisation and pathophysiological pathways of idiopathic childhood dystonia.

Anticonvulsants↗
PubMed1999

Sporadic amyotrophic lateral sclerosis of long duration mimicking spinal progressive muscular atrophy: a clinicopathological study.

We report an autopsy case of amyotrophic lateral sclerosis (ALS) clinically diagnosed as spinal progressive muscular atrophy (SPMA). The patient was a Japanese woman without hereditary burden. She developed muscle weakness of the distal part of the left lower extremity at age 42, followed by muscle weakness and atrophy of the right lower extremity and upper extremities. At age 57, she needed transient ventilatory support. Slight weakness in the facial muscles and fasciculation of the tongue appeared at age 60. At age 61, she died of sudden respiratory arrest. During the clinical course, neurological examination revealed neither Babinski signs nor hyperreflexia. The neuropathological examination revealed not only neuronal loss with gliosis in the facial nucleus, hypoglossal nucleus, and anterior horns of the spinal cord, but also loss of Betz cells and degeneration of the pyramidal tracts. Based on these clinicopathological findings and review of literature, we conclude that sporadic ALS mimicking SPMA is present.

Amyotrophic Lateral Sclerosis↗
PubMed1992

A new procedure for assessment of proprioception.

A new method for the assessment of proprioception was developed and tested with 40 healthy subjects on two facial muscles (i.e., masseter and zygomatic muscles). The experiment was repeated after 3 1/2 months. In our study, proprioception was studied with respect to sensations arising from the muscle spindles and tendon organs. Therefore, myesthesia was investigated, which was assessed by the correspondence between a voluntary muscle contraction and its immediate replication. Good perception was defined by a small integral of differences, standardized by duration and intensity of the contraction, and its replication. Results show that this measure is independent of the characteristics of muscle activation. In concordance with our hypothesis, myesthesia was superior in a muscle richly supplied with muscle spindles and afferent fibers (i.e., masseter muscle), to that for a muscle less prepared for afferent information processing (i.e., zygomatus major).

Adult↗
PubMed2001

[Clinical symptoms, diagnosis and treatment of focal dystonias].

Focal dystonias are relatively rare and significantly disabling disorders. These include cervical dystonia, blepharospasm and hemifacial spasm. The spasmodic torticollis consists of tonic posturing of the head away from its neutral position or twisting of the cervical muscles. The blepharospasm is an abnormal blinking, eyelid tic or twitch resulting from any cause. The hemifacial spasm is an involuntary unilateral twitching of the facial muscle. Patients affected by focal dystonias are predominantly females, and many times psychical stress can be revealed. The pathogenesis may involve dysfunction of the basal ganglia and brain stem although the exact mechanism remains to be elucidated. The patients need to be diagnosed and treated in centers specialized in movement disorders. Although many drug treatments can be beneficial, the most effective treatment is the local Botulinum toxin injection into the affected muscles. This neurotoxin produces temporary neuromuscular blockade, which reveals the symptoms and pain. The effect of the toxin is temporary and, therefore, the injection needs to be repeated every 6-12 weeks. The most common side effects are hypersensitivity, bleeding, hematoma, ptosis, facial spasm, dysphasia or dysarthria. With the use of proper dose and injection sites these side effects can be avoided.

Anti-Dyskinesia Agents↗
PubMed2002

[Indications for labial reanimation in facial paralysis].

The therapeutic approach of labial reanimation depends on several points, like the association with others abnormalities, the palsy which can be complete or partial, the age of the patient and the practice of the surgical team. Nevertheless, the authors try to propose a surgical approach of labial reanimation in facial palsy, depending on the facial nerve which can be reparable or not, and on the facial muscles which can be used or not. At least, the indications in partial labial palsy are recalled.

Adult↗
PubMed1983

Peripheral facial palsy with intact taste and tearing caused by intrapontine lesion.

Two patients with documented lesions in the floor of the fourth ventricle had unilateral paralysis of the upper and lower facial muscles but normal taste sensation and tearing function. These findings contradict the widely accepted clinical notion that an intraparenchymal lesion of the facial nerve invariably causes loss of gustatory and lacrimal function.

Brain Diseases↗
PubMed2005

Study on remodeling of astrocytes in facial neuclus after peripheral injury.

To observe the glial reactions surrounding facial motor neurons following facial nerve anastomosis. At 1, 7, 21 and 60 d following facial nerve anastomosis, the recovery process of facial movement was observed, the glial fibrillary acidic protein (GFAP) immunoreactivity was analyzed by a combined method of fluorescent retrograde tracing and immunofluorescent histochemical staining, and the ultrastructure of astrocytes were observed under a transmission electron microscope (TEM), respectively. Postoperatively the function of facial muscles could not return to normal, often accompanied with hyperkinetic syndromes such as synkinesis at the late stage. Motor neurons in every facial subnucleus could be retrogradely labeled by fluoro-gold (FG), and displayed an evident somatotopic organization. Normally there was a considerable number of GFAP-positive cells in nonnucleus regions but few inside the facial nucleus region. Postoperatively the GFAP immunoreactivity in the anastomotic side increased significantly, but gradually decreased at the late stage. The ultrastructure of astrocytes in our experiment showed that the sheet-like process of astrocytes invested and protected the injured facial motor neurons. The present study shows that reactive astrocytes undergo some characteristic changes during the process of facial nerve injury and regeneration. The plastic change at the late stage may be involved in the mechanism of synkinesis.

Animals↗
PubMed1990

Complete external ophthalmoplegia in a patient with congenital myopathy without specific features (minimal change myopathy).

An 11-month-old female infant with mild asphyxia at birth had severe generalized muscle hypotonia and weakness, predominantly in the neck flexors, a high-arched palate and a funnel chest from early infancy. Her facial muscles were also markedly involved. In addition, she showed striking non-progressive, complete external ophthalmoplegia and mild ptosis. A muscle biopsy specimen showed non-specific myopathic changes, including mild variation in fiber size, mild type 1 fiber predominance, type 2B fiber deficiency and slightly increased acid phosphatase activity. Complete ophthalmoplegia may thus be seen not only in myotubular myopathy but also in various forms of congenital non-progressive myopathy.

Abnormalities, Multiple↗
PubMed2004

The motor cortex and facial expression: new insights from neuroscience.

BACKGROUND: For more than a century, unusual and complex deficits in facial expression have been known to occur following localized brain damage. Some brain injuries leave the face with pronounced alterations in affect whereas others result in movement disorders such as blepharospasm and Meige syndrome. There is also a historic trail of clinical observations that document deficits in either voluntary or emotional control of the facial muscles following central nervous system damage. REVIEW SUMMARY: Recent studies in the nonhuman primate cerebral cortex reveal the existence of multiple cortical facial representations in the frontal lobe and adjacent anterior cingulate cortex. These comprise the facial representation of the primary motor cortex (M1), ventral lateral premotor cortex (LPMCv), supplementary motor cortex (M2), rostral cingulate motor cortex (M3), and caudal cingulate motor cortex (M4). Homologous facial representations reside in the human brain based on observations following cortical stimulation, functional neuroimaging, and localized surgical resection. In the nonhuman primate, all these facial representations have been found to be directly interconnected through topographically organized corticocortical connections, and each facial area has also been found to send direct corticobulbar projections to the facial motor nucleus. The facial representations of M2 and M3 are both located on the medial wall of the hemisphere, in the vascular territory of the anterior cerebral artery. Both preferentially give rise to bilateral projections to parts of the facial nucleus that innervate the upper facial musculature as demonstrated in the monkey. The facial representation of M1, LPMCv, and M4 preferentially give rise to contralateral axonal projections ending in parts of the facial nucleus that innervate the lower facial musculature. The facial representation of M1 and LPMCv both reside in the vascular territory of the middle cerebral artery (MCA). The classic clinical presentation of paralysis in the contralateral lower facial musculature and intact bilateral upper facial musculature following typical MCA in infarction in the human parallels this mapping pattern of corticobulbar connections found in the nonhuman primate. CONCLUSIONS: Facial movements are undoubtedly under the powerful influence of the cerebral cortex and are essential for the appropriate execution of many important functions such as mastication, swallowing, and social interaction, including speech and nonverbal communication. This information provides a theoretic template for interpreting the clinical effects of neuropathologic disease and localized cortical trauma on facial movements.

Animals↗
PubMed1985

[Nuclear magnetic resonance imaging in a case of facial myokymia with multiple sclerosis].

A 59-year-old female of facial myokymia with multiple sclerosis was reported. In this case, facial myokymia appeared at the same time as the first attack of multiple sclerosis, in association with paroxysmal pain and desesthesia of the neck, painful tonic seizures of the right upper and lower extremities and cervical transverse myelopathy. The facial myokymia consisted of grossly visible, continuous, fine and worm-like movement, which often began in the area of the left orbicularis oculi and spread to the other facial muscles on one side. Electromyographic studies revealed grouping of motor units and continuous spontaneous rhythmic discharges in the left orbicularis oris suggesting facial myokymia, but there were no abnormalities on voluntary contraction. Sometimes doublet or multiplet patterns occurred while at other times the bursts were of single motor potential. The respective frequencies were 3-4/sec and 40-50/sec. There was no evidence of fibrillation. The facial myokymia disappeared after 4-8 weeks of administration of prednisolone and did not recur. In the remission stage after disappearance of the facial myokymia, nuclear magnetic resonance (NMR) imaging by the inversion recovery method demonstrated low intensity demyelinated plaque in the left lateral tegmentum of the inferior pons, which was responsible for the facial myokymia, but X-ray computed tomography revealed no pathological findings. The demyelinated plaque demonstrated by NMR imaging seemed to be located in the infranuclear area of the facial nerve nucleus and to involve the intramedurally root.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1995

[A 65-year-old woman with dysarthria, dysphagia, weakness, and gait disturbance].

We report a 65-year-old woman with progressive dysarthria, dysphagia, weakness, and gait disturbance. The patient was well until 59 years of age (January of 1986) when she noted bilateral ptosis. One year later, she noted a gradual onset of difficulty in speech (articulation). Her speech slowly deteriorated and she noted weakness in chewing power and difficulty in swallowing in addition. In October 1987, she developed emotional incontinence. In January of 1988, she started to drag her left foot. She was admitted to our hospital on June 13 of 1988. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed no dementia; her higher cerebral functions appeared intact. Ptosis was present bilaterally more on the right. She showed difficulty in opening her eyes on command; no contraction of the frontal muscles was seen upon attempted eye opening. There was a moderate limitation in the vertical gaze. Forced laughing and crying were seen. Facial muscles were moderately weak without apparent atrophy. The movement of the soft palate was very weak, and swallowing disturbance was more prominent for liquid staff. The tongue appeared somewhat small, however, no fasciculation was noted. Her step was small and the posture was stooped. Retropulsion was present, however, Romberg's sign was absent. No muscle atrophy was apparent, however, diffuse mile to moderate muscle weakness was noted in all four limbs. Cerebellar sign was absent. Deep tendon reflexes were exaggerated bilaterally, and Babinski sign was present on the left side. Sensation was intact. Routine blood tests were unremarkable as was a cranial CT scan. Her ptosis did not improve after 10 mg of edrophonium injection. CSF was also normal. She was transferred to another hospital but her neurological disabilities further progressed. In 1989, she was totally unable to move her limbs; she could only move her eyes; still consciousness was clear without dementia. She developed respiratory difficulty and expired on July 25, 1992. She was discussed in a neurological CPC, and the opinions were divided into ALS and primary lateral sclerosis (PLS). The chief discussant arrived at the conclusion that the patient might have had the pyramidal form of ALS. Postmorten examination revealed marked myelin pallor in the anterior as well as lateral corticospinal tracts. Pyramidal tract degeneration was prominent starting at the level of the cerebral peduncle and was continued to be seen until the level of lumbar cord. The number of anterior horn cells showed only slight decrease in the cervical level, however, it was normal in the lumbar cord.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1979

The role of facial response in the experience of emotion.

Facial expression and emotional stimuli were varied orthogonally in a 3 x 4 factorial design in order to test whether facial expression is necessary or sufficient to influence emotional experience. Subjects watched a film eliciting fear, sadness, or no emotion, while holding their facial muscles in the position characteristic of fear or sadness, or in an effortful but nonemotional grimace; those in a fourth group received no facial instructions. The subjects believed that the study concerned subliminal perception and that the facial positions were necessary to prevent physiological recording artifacts. The films had powerful effects on reported emotions, the facial expressions none. Correlations between facial expression and reported emotion were zero. Sad and fearful subjects showed distinctive patterns of physiological arousal. Facial expression also tended to affect physiological responses in a manner consistent with an effort hypothesis.

Arousal↗
PubMed1992

Tinnitus of TMJ origin: a preliminary report.

Twenty patients whose chief complaint was tinnitus were examined. They were not known to have temporomandibular disorders. They did not have pain or dysfunction. They were examined by physicians for ear disorders and the results were considered negative. Each of these patients had a complete history and clinical temporomandibular joint examination. The clinical examination included muscle and joint palpation and stethoscopic examination of the joint. This examination also included selected computerized mandibular scans and electromyographic studies of selected facial muscles. Each subject had eight views of transcranial lateral oblique x-rays taken. It was determined that 19 of these individuals had one or more clinical, electromyographic, and radiographic indications of a temporomandibular disorder. From this study, it appears that individuals who have tinnitus with no apparent otologic basis for this symptom should have a careful evaluation of the temporomandibular apparatus. A temporomandibular disorder may be one of the primary causes of this symptom.

Adult↗
PubMedDate not supplied

[Hereditary sensorimotor neuropathy in electrophysiological studies].

We performed clinical and electrophysiological studies in 42 children with hereditary motor and sensory neuropathy type I and II (HMSN I and II) and in 103 members of their families. In 24 families with HMSN I the conduction velocity and latency were markedly changed in the nerves innervating the distal muscles (median, peroneal nerves) as well as proximal muscles (facial, axillary and musculocutaneous nerves). The changes were uniform in all motor and sensory nerves studied in a particular patient. The intensity of changes was similar in members of their families even when the clinical abnormalities were minimal, thus the degree of conduction velocity slowing was uniform within families. In adults with HMSN I (group A i B) we found less marked slowing of nerve conduction as compared to children (group P), the difference being significant (p < 0.001). It may suggest a slow process of peripheral nerves maturation despite the existing morbid condition. In patients of 18 families with HMSN II slight changes in conduction velocity were found only in nerves innervating the distal muscles, more evident in legs (peroneal and sural nerves). Conduction time of facial, axillary and musculo-cutaneous nerves was normal. The values of nerve conduction were not changing with patients' age. We recommend examining conduction time in facial, axillary or musculocutaneous nerve as a useful procedure for differentiation between HMSN I and II, especially in families with borderline conduction values in the nerves innervating distal muscles.

Adult↗
PubMedDate not supplied

Muscular and CNS effects of carotid artery administration of contrast media in rabbits.

Facial muscle twitching during intracarotid injections of nonionic contrast media has been observed in rabbits. To investigate the cause of this reaction, cortical EEG and facial EMG recordings were made from rabbits receiving selective internal and external carotid artery injections of control solutions (normal saline, mannitol), an ionic contrast medium (meglumine iothalamate), and three nonionic contrast media (iohexol, iopromide, and iotrolan). Internal carotid artery injections with all contrast media, both ionic and nonionic, produced ipsilateral EEG changes in 24 of 28 animals; however, ipsilateral EMG changes and visible twitching were observed only in animals injected with nonionic contrast media. Internal carotid artery injections with control ionic and nonionic solutions (physiological saline and mannitol, respectively) produced no EEG changes in any animals. Mannitol produced only ipsilateral EMG changes and visible twitching in most animals. The severity of the reaction to mannitol was generally less than that to the nonionic contrast media, and this difference was statistically significant when comparing mannitol with iohexol and iotrolan but not with iopromide. External carotid artery injections with nonionic solutions (contrast media and mannitol) produced significantly more severe ipsilateral EMG changes and visible twitching than were recorded with the internal carotid artery injections. Ionic solutions (contrast media and saline) had no effect. EEG changes were not observed after external carotid artery injection of any solution, with the exception of two of the seven animals injected with iotrolan. Angiography demonstrated retrograde filling of the external carotid arterial system from internal carotid artery injection via functioning orbital anastamoses. In contrast, internal carotid arterial vessels were not seen angiographically after external carotid artery injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Gardner neurovascular decompression of the trigeminal and facial nerves for tic douloureux and hemifacial spasm.

Neurovascular decompression of the trigeminal and facial nerves for tic douloureux and hemifacial spasm has been performed for the past two decades, starting with W. James Gardner in 1959. Although other neurosurgeons have refined and further perfected the operation, reporting large series of successful results, the credit for the concept and original procedures, including use of the surgical microscope, has generally escaped the attention of present-day neurological surgeons. This paper attempts to correct this inequity.

Facial Muscles↗