Neurosarcoidosis presenting as major depression.
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Biomedical subjects
Publications and source records attributed to M B Bender.
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Tests for graphesthesia and for directional cutaneous kinesthesia (DCK) were performed on a large series of neurological patients and normal subjects, in addition to the standard tests for discriminative sensation. Defects in graphesthesia and DCK were found with lesions at all levels of the nervous system. Graphesthesia was more often and more severely affected than DCK. These functions when impaired were always associated with other sensory defects (directional joint kinesthesia, two-point discrimination, etc.) in different combinations. It appears DCK is probably the basis for graphesthesia. Recent experimental studies have provided an anatomic and physiologic basis for DCK and for graphesthesia. These studies have also discredited wide-held beliefs on the transmission of discriminative sensation through the spinal cord. In this light, the history of ideas about sensation and its mediation is reviewed, and it is concluded that DCK alone deserves to be called a "posterior column function". Graphesthesia and DCK are discussed as kinesthetic functions implying orientation in cutaneous sensory space. These are compared to stereognosis and braille reading, which are complex derived functions depending also on motion, but directed towards recognition in external haptic space. Graphesthesia and DCK should both be considered as distinct forms of somatic sensibility which are valuable adjuncts to the clinical sensory examination.
(1) It appears that all oculomotor pathways originating within the cerebrum and mediating stimulations and lesions, project from the two sides of the brain through the diencephalon to the brain-stem. (2) The pathways subserving horizontal movements decussate at the level of the oculomotor and trochlear nuclei, across the midsagittal plane. The direction of vector action within the brain above the 'electroanatomical' oculomotor decussation is predominately contraversive; below this levelit is ipsiversive. (3) The pontine reticular formation, the abducens and oculomotor nuclei and the median longitudinal fasciculus play an important role in the physiology of ipsilateral conjugate gaze. A 1 mm lesion within the paramedian pontine reticular formation causes paralysis of ipsilateral conjugate gaze, while a 1 mm lesion within the median longitudinal fasciculus causes impairment of contralateral (disconjugate) gaze with paralysis of adduction of the ipsilateral eye and nystagmus in the contralateral or abducting eye. (4) True binocular vertical movements occur only when both sides of the brain are activated either directly or through bilateral sensory (visual or vestibular) inputs. Vertical and oblique monocular movements can be elicited on unilateral stimulation at the level of the oculmotor nucleus. (5) Paralysis of vertical gaze is caused by bilateral lesions. Bilateral (1 to 2 mm) lesions within the region of the rostral interstitial nucleus of the median longitudinal fasciculus result in isolated paralysis of downward gaze. More caudally, bilateral (1 mm) lesions within the pretectum or midsection of the posterior commissure result in paralysis of upward gaze. (6) In different regions of the brain a theoretical transverse plane can be drawn between pathways which transmit impulses for vertical eye movements. Those which transmit impulses for binocular downward movement are situated dorsal to this plane, while those that trasmit impulses for upward movement are located ventrally to this plane. This topographical relationship can be demonstrated in the occipital lobe and to some extent in the frontal lobes. A hypothetical transverse plane separating the down and up eye movement can also be drawn at the mesodiencephalic junction. At the level of the oculmotor nucleus stimulations at the most rostral pole result in monocular downward movements, while the most caudal pole stimulations produce monocular upward movements. There is no evidence that the pathways which mediate binocular upward and binocular downward movement project across a hypothetical transverse plane. (7) Our knowledge of the synaptic connections between the cerebrum, diencephalon and the brain-stem nuclei, especially the paramedian pontine reticular formation, involved in binocular movements remains incomplete. Moreover, the anatomical location of the decussation of the right and left cerebral pathways which transmit conjugate eye movements are still unknown...
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Ten monkeys were stimulated unilaterally and bilaterally through bipolar electrodes placed stereotactically on each side of the midline under light barbiturate anaesthesia. Bilateral simultaneous stimulation elicited straight downward binocular movements from a core of tissue about 40 mm3 on each side which included the fields of Forel, zona incerta, subthalamic nucleus, oral pole of the red nucleus, fasciculus retroflexus and 'area tegmentalis'. Unilateral stimulation of the same points yielded downward eye movements in only 25 per cent of the instances. Upward deviation of the globes could be elicited by bilateral stimulation of tissue located more caudal, ventral and medial than that from which downward movements were obtained. Bilateral electrolytic lesions within the region outlined above caused significant defects in downward gaze both in saccadic and slow pursuit binocular movements. Passive bending of the head backwards, however, resulted in downward deviation of the globes (oculocephalic reflex). Optokinetic nystagmus and after-nystagmus downward were abolished. Oblique (45 degrees) optokinetic stimulation elicited a perverted response in the horizontal plane. Vestibulo-ocular reflexes elicited by bilateral warm irrigation of both ear canals with the monkey in the erect position, or by turning the animal while lying on one side, caused a strong tonic deviation upward with absence of nystagmus downward. Some of these monkeys showed additional alterations in upward gaze but they were less severe in intensity and duration than those of downward gaze. All eye deviations in the horizontal plane were consistently normal. Recovery occurred in all types of vertical binocular movements except in the rapid motions (saccades and quick phases of nystagmus) below the horizontal meridian. A unilateral lesion had no effect. The minimal damage producing downward gaze defects was about 1.7 mm in diameter, cetred in the prerubral fields, rostral and medial to the red nuclei with minimal involvement of the oral pole of these structures. The nuclei of Cajal, Darkschewitsch and interstitialis of the posterior commissure, as well as the fasciculus retroflexus and the posterior commissure, were spared by this lesion. The so-called rostral interstitial nucleus of the medial longitudinal fasciculus and the nucleus campi Foreli appear to be destroyed. These structures are known to receive an input from the paramedian pontine reticular formation and project on to the oculomotor nerve nucleus. These results demonstrate that the prerubral fields contain structures which are critical for rapid eye movements downward, and therefore an isolated downward gaze palsy is a strong indicator of a bilateral lesion of this zone. The findings in the few reported cases with this sign and available pathological analysis suggest that our conclusions from the experimental monkey apply to man as well. The concept of bilateral innervation for vertical eye movements is amply confirmed for the downward vectors...
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Characteristic visual symptoms and signs in 12 patients with neoplasms or aneurysms involving the optic tract are summarized. Blurred vision was the most common initial manifestation. Optic atrophy became apparent in 7 of the 12 patients. Most patients had uniocular central scotomas with reduced visual acuity, and 2 had homonymous scotomas. Field defects were frequently incomplete and incongruous, combining central scotomas with elements of homonymous and bitemporal amblyopias. Seven patients had endocrine disturbances and memory deficits in addition to their visual symptoms.
Six recent and six long-term follow-up patients with subdural hematoma studied by computer assisted tomography are reported. This method was used to demonstrate progressive resolution of the hematoma in five of the recent patients as well as enlargement of the hematoma in one of the patients who subsequently was sent to surgery. Computer assisted tomography was also used to demonstrate absence of subdural hematoma in long-term follow-up of unoperated patients. The possible difficulty in visualizing an isodense subdural hematoma is discussed, as is the use of additional coronal views to improve subdural detection.
An infant born with severe but nonprogressive somatic and cranial muscle weakness including bilateral external ophthalmoplegia was studied with a motor-point muscle biopsy. There was a strinking generalized decrease in the size of muscle fibers (hypotrophy), most marked in the type I fibers. Many of the small fibers were immature, resembling myotubes. Neuromuscular junctions on severely hypotrophic fibers were normal with esterase staining and by ultrastructural criteria. Although these are unusual clinical and biopsy characteristics, this infant's condition bears a resemblance to two other congenital nonprogressive neuromuscular diseases:myotubular myopathy and congenital fiber type disproportion. In these conditions and in our patient, there is no primary degenerative process affecting nerve or muscle but, rather, an apparent lack of maturation of fetal muscle fibers, indicating a defective normal trophic interaction between nerve and muscle.
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The effects of eyelid closure on oculomotor function was examined in 11 patients with palatal myoclonus. In eight patients, eyelid closure induced gross rhythmic vertical or almost oscillatory movements of the globes, which were synchronous with the rhythmic beat of the palatal myoclonus. The rhythmic vertical ocular movements induced by eyelid closure replaced calorically induced or spontaneous horizontal nystagmus present when the lids were open. Vertical ocular motions persisted during some stages of slow-wave sleep and reappeared during each stage of rapid eye movement. The physiologic basis of the palato-ocular synchrony may be similar to the eyelid closure, vertical eye movements, and palatal myoclonus that occurs in monkeys on stimulation of the central tegmental fasciculus.
The authors report nine patients selected from over 100 patients with subdural hematomas successfully treated without surgery. These patients were followed for as long as 5 years. All had angiographically demonstrated subdural hematomas. Electroencephalograms (EEG) documented well the clinical improvement of the patient, but were poor guides to the true size of the hematoma, since EEG returns to normal early in the patient's course. Static scans are a better guide to the presence of a subdural hematoma, but they lag behind clinical improvement and usually remain abnormal for considerable periods of time after a major portion of the hematoma has been reabsorbed, and the patient is asymptomatic.
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A bright pocket flashlight was directed into one eye for 10 seconds; the subject then closed the eyelids and reported the sequence of after-image colours observed. Lesions of the visual system which compromised bilateral central colour vision also reduced or abolished the `flight of colours'. This simple bedside test of each eye independently is of value in detecting mild defects of central vision.
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