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.

Presentation of an unusual case of sarcoidosis causing Homer's syndrome with multiple cranial neuropathies including bilateral sensorimotor trigeminal and spinal accessory neuropathies. Other neurologic manifestations included bilateral hypoglossal neuropathies and a thoracic myelopathy with a normal myelogram. A CT scan showing enhancing calcifications in the basal cisterns is compared with those described in the literature.

On correlating the clinicopathologic data in man with those in the experimental monkey one may conclude that the syndrome of paralysis of upward gaze is due to involvement of the mesencephalon, while the syndrome of paralysis of downward gaze is due to implication of a more rostral area in the diencephalon. In instances of paralysis of both upward and downward gaze the pathology is at the mesodiencephalic junction. Paralysis of downward gaze is rarely associated with impairment of pupillary reflexes, whereas paralysis of upward gaze is frequently accompanied by impairments of efferent pupillary responses, eyelid retraction and, less frequently, by binocular adductive saccades. In man, paralysis of upward gaze is commonly caused by lesions, such as tumor, vascular disease or aqueductal stenosis, localized within the mesodiencephalon. Isolated paralysis of downward gaze is rare in cases of tumor and found predominately in patients with vascular disease. In patients with diffuse involvement of the brain, such as lysosomal storage disease or progressive supra-nuclear palsy, paralysis of vertical gaze is common and almost always bidirectional with impairment of downward preceding that of upward gaze. The defects in saccades in all of these cases precede impairment of pursuit or smooth movements. Obliquely induced eye movements, in patients or monkeys with paralysis of vertical (upward or downward) gaze. resulted in horizontal nystagmus. Binocular adductive saccades and questionable 'retractory nystagmus' may be found in patients with paralysis of upward gaze due to tumor or vascular lesion of the mesodiencephalic area or in cases of acute distention of the oral portion of the aqueduct of Sylvius. The binocular adductive saccades. which can be induced by attempts to look upward. or during induction of ocular gaze nystagmus in an upward or obliquely upward direction (with optokinetic or vestibular stimuli). remain unexplained.

(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...

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...

Many patients with aphasia or an organic mental syndrome who can spell a five-letter word or recite a five-digit number forward fail to do so backwards. Errors also occur in reading letters of a printed word backwards whereas no errors appear in reading conventionally. Memory defects, dysnomia, dyscalculia, learning disorders, and perseveration may co-exist with an impaired ability to reverse a serial order of symbols. It would appear that a defect in the ability to reverse a serial order may be similar to defects in other faculties observed in aphasia, e.g. anomia, acalculia, and alexia. Reversability is probably a characteristic of normal cognitive function and language processes. A defect in RS of two-, three-, or four-letter words may be considered a significant sign of cerebral dysfunction due to either a localized lesion in the dominant hemisphere or a diffuse bilateral encephalopathy.

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.

In Reply.— Our article does not deal with the question of whether or not Bell phenomenon occurs during spontaneous blinks of short duration. We made no attempt to analyze oculomotor activity during blinking. We studied the effects of eyelid closure on oculomotor function in patients with palatal myoclonus. Vertical ocular motions synchronous with the beat of the palatal mvoclonus occurred only during "volitional" prolonged eyelid closure or attempted closure against resistance. These eye motions were a specific effect of active continuous eyelid closure and could not be obtained by sensory-induced reflex eyelid closure. The ocular excursions were recorded by DC electro-oculogram. Both voluntary blinking and eyelid fluttering while the lids are closed have a typical appearance on the DC EOG. Neither blinking nor eyelid fluttering interferes with accurate recordings of the position and movements of the globes beneath the closed lids by DC EOG. The angular motion of the eye can be

✓ 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.

Many of the features of palinacousis analyzed in this report suggest that these auditory perceptual illusions are, in themselves, clinical manifestations of seizure activity. Additional evidence presented in support of this hypothesis includes observed correlations of the episodic palinacoustic experiences with other spontaneous paroxysmal symptoms and the similarity of these phenomena to sensory illusions evoked by electrically stimulating the temporal lobes of conscious man. The relationship between palinacousis and analogous perceptual illusions in different modalities leads us to propose that other episodic perseverative sensory illusions, including palinopsia, may also be seizure phenomena.

The pattern of alteration of the corneo-fundal potential (CFP) of the human eye during the night of sleep was found to be similar in 15 subjects. During the first 30 min of entry into darkness and the onset of sleep CFP alterations were of large magnitude. A 28% decrease was followed by a 49% increase above the CFP level in standard illumination. These changes are probably a reflection of the process of dark adaptation of the retina. They are not influenced by the level of alertness. Throughout the remainder of the night of sleep the CFP changes are reliable and predictable. After the first hour the level of CFP is only slightly above that in bright illumination prior to sleep onset. Between 1.5 and 6 h the CFP increases in a linear manner. Once the level after 90 min is determined, the actual level after 6 h may be accurately predicted utilizing a linear model. Thus, for practical purposes the sensitivity of the amplifier of a DC recording system may be fixed after the initial pre-sleep calibration in standard room lighting and the level of elevation noted after 90 min.

ABSTRACTAs a result of recording eye movements during Stage REM sleep by AC electrooculography (EOG) previous investigators concluded that each eye movement is the response to the visual action in each dream. When we repeated the study using DC EOG it was discovered that only a minority of eye movements during Stage REM are in the direction of the visual action in the dream. If only single, large amplitude, prominent eye movements are considered then most such movements are related to colorful, compelling visual action occurring as a prominent single visual action against a quiet background. The AC recording method used in past studies emphasizes these isolated movements; perhaps this explains the disparity in results. At any rate, most eye movements during REM sleep are unrelated to the action in the dream. When these eye movements were analyzed in regard to the direction of movements, sequential order of movements, and randomness in time, we found that similar patterns of oculomotor output were found in all subjects. Thus, the nervous system executes a patterned output of oculomotor activity during dreaming sleep which is fairly consistent in all subjects. At times, however, a link is established between the visual and oculomotor systems and the eyes respond to visual action.