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Biomedical subjects

D N Levine

Publications and source records attributed to D N Levine.

At least 19 recordsLinked to original sources
PubMed2001

The pathophysiology of lumbar puncture headache.

The pathophysiology of lumbar puncture headache (LPH) is still unclear. There is evidence that leakage of cerebrospinal fluid (CSF) leads to CSF hypotension, which causes dilation of intracranial veins, resulting in LPH. However, CSF leaks at the skull base are not associated with orthostatic headache; there is poor correlation between recumbent CSF pressure and LPH; and there has been no satisfactory explanation of how venous dilation causes orthostatic headache. We propose the hypothesis that LPH is caused by an abnormal distribution of craniospinal elasticity. Increased compliance at the lumbar end of the spinal CSF space, resulting both from anatomic joining of the subarachnoid to the epidural space and from reduced CSF filling pressure, causes the hydrostatic indifferent point to move caudally, creating additional intracranial hypotension and venous dilation in the erect position. We are, thus, able to explain the orthostatic character of LPH, the fact that spinal but not cranial sites of leakage produce orthostatic headache and the imperfect correlations both between recumbent CSF pressure and LPH and between reduced CSF volume and LPH. The near absence of LPH in the very young and in the elderly relates to the relative stiffness of the epidural space at these ages. Epidural injections of blood or saline give immediate relief by reducing epidural distensibility.

Age Factors↗
PubMed2000

Ventricular size in pseudotumor cerebri and the theory of impaired CSF absorption.

The purpose of this theoretical study is to determine whether the absence of ventricular enlargement in pseudotumor cerebri (PTC) is consistent with the theory that PTC is caused by reduced absorption of cerebrospinal fluid (CSF), either from increased outflow resistance at the arachnoid villi or from obstruction of the dural venous sinuses. We model the brain as a thick spherical shell of parenchyma, enclosing a CSF-filled ventricular system, and surrounded by a thin cerebral subarachnoid space (CSAS). We treat the parenchyma as a porous solid matrix, filled with interstitial fluid and blood vessels. We subject the model to a uniform increase in CSF pressure (CSFP) and solve the equations of poroelasticity for the resulting displacements of parenchymal tissue. The effect of a rise in CSFP on ventricular size depends on the response of the cerebral blood vessels and the degree to which the pia is tethered to the dura. If the cerebral vessels decrease in caliber with increasing CSFP, a rise in CSFP causes the ventricles to contract and the CSAS to expand if the pial surface is free to move inward, but causes slight ventricular enlargement if the pia is tethered to the dura. If, instead, the vessels dilate, the ventricles contract and the CSAS becomes effaced. Small, normal, or slightly enlarged ventricles in PTC are consistent with the theory of reduced CSF absorption.

Brain Neoplasms↗
PubMed1998

Spontaneous pulsation of the retinal veins.

The classical theory of spontaneous pulsation of the retinal veins is that during systole intraocular pressure exceeds venous pressure, causing the veins to collapse. We show that this theory is internally inconsistent and not in accord with experimental data. It is inconsistent in assuming both (a) that oscillations of intraocular pressure (IOP) occur because the veins cannot immediately discharge the systolic arterial inflow and (b) that retinal venous pressure (RVP) can fluctuate independently of IOP during the cardiac cycle. It is not in accord with experimental data, which shows that RVP always exceeds IOP and that fluctuations in the latter are instantly transmitted to the former. We present an alternative theory that does not have these problems. We assume the following. (1) Inflow to the retinal venous tree from the capillaries is constant, the pulsatile arterial flow having been completely damped by the arterioles and capillaries. (2) Outflow from the central retinal vein (CRV) varies during the cardiac cycle because oscillations of IOP, transmitted to the intraocular CRV, are of greater amplitude than oscillations in cerebrospinal fluid pressure, transmitted to the extraocular CRV. By showing that the radial blood flow distending the veins obeys a diffusion equation and by employing an "equivalent cylinder" analysis of the branched venous tree to simplify the boundary conditions, we demonstrate that, with the above assumptions and the additional assumption of low amplitude of radial flow, the CRV will pulsate, and the pulsations will remain confined to a small segment near the exit point. The proposed theory can explain disappearance of pulsation with intracranial hypertension, intensification of pulsation in glaucoma, and variability in the linear extent and amplitude of pulsation among normal individuals. The theory may also be applied to other venous pulsations, such as the respiratory pulsation of the terminal portions of large veins entering the thorax or the cardiac cycle pulsation of the superior vena cava.

Animals↗
PubMed1997

Pathogenesis of cervical spondylotic myelopathy.

OBJECTIVE: To determine whether either of two mechanical theories predicts the topographic pattern of neuropathology in cervical spondylotic myelopathy (CSM). The compression theory states that the spinal cord is compressed between a spondylotic bar anteriorly and the ligamenta flava posteriorly. The dentate tension theory states that the spinal cord is pulled laterally by the dentate ligaments, which are tensed by an anterior spondylotic bar. METHODS: The spinal cord cross section, at the level of a spondylotic bar, is modelled as a circular disc subject to forces applied at its circumference. These forces differ for the two theories. From the pattern of forces at the circumference the distribution of shear stresses in the interior of the disc-that is, over the transverse section of the spinal cord-is calculated. With the assumption that highly stressed areas are most subject to damage, the stress pattern predicted by each theory can be compared to the topographic neuropathology of CSM. RESULTS: The predicted stress pattern of the dentate tension theory corresponds to the reported neuropathology, whereas the predicted stress pattern of the compression theory does not. CONCLUSIONS: The results strongly favour the theory that CSM is caused by tensile stresses transmitted to the spinal cord from the dura via the dentate ligaments. A spondylotic bar can increase dentate tension by displacing the spinal cord dorsally, while the dural attachments of the dentate, anchored by the dural root sleeves and dural ligaments, are displaced less. The spondylotic bar may also increase dentate tension by interfering locally with dural stretch during neck flexion, the resultant increase in dural stress being transmitted to the spinal cord via the dentate ligaments. Flexion of the neck increases dural tension and should be avoided in the conservative treatment of CSM. Both anterior and posterior extradural surgical operations can diminish dentate tension, which may explain their usefulness in CSM. The generality of these results must be tempered by the simplifying assumptions required for the mathematical model.

Cervical Vertebrae↗
PubMed1993

The visual variant of Alzheimer's disease: a clinicopathologic case study.

A 59-year-old man developed problems with reading and driving. When first examined, he had great difficulty locating and identifying items by sight. Visual acuity was normal, but contrast sensitivity for low spatial frequencies was severely impaired. The peripheral visual fields were moderately constricted with depressed flicker fusion frequencies, more on the right. Color identification was preserved. The difficulties in identifying and locating objects by sight were aggravated by increasing the complexity and multiplicity of the items in the field of vision and by changing the ambient illumination. Intellect and memory were relatively intact, except for difficulty with calculations. Over a 12-year course the visual defects steadily worsened, and eventually memory and language skills failed. Social manners, perseverance, and affect remained normal. Postmortem examination showed cortical atrophy, predominantly posterior, with abundant neurofibrillary tangles and senile plaques. The density of the tangles was correlated with the severity of the atrophy, being highest in the occipitoparietal areas and lowest in the frontal lobes. Alzheimer's disease can preferentially affect the posterior cerebral hemispheres and cause a dementia presenting with, and dominated by, visual disturbances.

Alzheimer Disease↗
PubMed1991

The pathogenesis of anosognosia for hemiplegia.

We compared patients with unawareness of hemiplegia lasting more than 1 month after right hemisphere stroke with other patients with right hemisphere stroke who became aware of hemiplegia within a few days after onset. Patients with persistent unawareness invariably had severe left hemisensory loss and usually had severe left spatial neglect. They were almost always apathetic; their thought lacked direction, clarity, and flexibility, and they had at least moderate impairment of intellect and memory. Their right hemisphere strokes were large and always affected the central gyri or their thalamic connections and capsular pathways. In addition, there was evidence of at least mild left hemisphere damage, most commonly caused by age-associated atrophy. The pathogenesis of anosognosia for hemiplegia may involve failure to discover paralysis because proprioceptive mechanisms that ordinarily inform an individual about the position and movement of limbs are damaged, and the patient, because of additional cognitive defects, lacks the capacity to make the necessary observations and inferences to diagnose the paralysis. We discuss the implications of this "discovery" theory and contrast it with other explanations of anosognosia.

Affect↗
PubMed1991

Reappearance of the visual percept after intentional blinking in a patient with Balint's syndrome.

We present a patient with Balint's syndrome who complained of fading of the scenes under visual fixation. When he intentionally blinked, the faded visual percept reappeared. The disappearance of the visual percept may be explained as the result of either unstable visual fixation or of saturation of the visual pathways. The role of blinking in reviving the visual percept may be explained accordingly as causing a refixation of the target under visual fixation or as resetting the visual pathways for visual processing.

Aged↗
PubMed1990

Peduncular hallucinosis associated with isolated infarction of the substantia nigra pars reticulata.

We report the clinicopathological study of an 83-year-old man who abruptly developed complex visual hallucinations, disordered sleep, and mild cognitive impairment that persisted until his death 6 months later. Postmortem neuropathological examination including serial sections through the diencephalon, midbrain, and pons disclosed isolated bilateral infarcts confined to the medial substantia nigra pars reticulata. The findings suggest that destruction of the pars reticulata may be the essential feature to the development of peduncular hallucinosis.

Aged↗
PubMed1990

Impaired verbal reasoning and constructional apraxia in subjects with right hemisphere damage.

In addition to causing visuospatial deficits, damage to the right cerebral hemisphere also impairs other cognitive abilities, including those requiring higher-order aspects of language. The present study used a standardized test battery to examine the relationship between visuospatial abilities and comprehension of narrative material in subjects having unilateral right hemisphere damage (RHD). In a series of 41 consecutively admitted RHD subjects, impairments in abstracting information from narrative passages were as prevalent and as severe in magnitude as constructional apraxia. Moreover, the extent of the visuospatial and linguistic impairments were highly correlated. Although age, educational levels, and degree of premorbid brain atrophy were all found to influence performance, analysis of a select subgroup of the population established that the covariation of visuospatial and verbal impairments is related to right hemisphere damage per se. Clinically, these findings may be of significance for understanding the pervasive cognitive impairments that are often evidenced by RHD patients.

Aged↗
PubMed1990

Unawareness of visual and sensorimotor defects: a hypothesis.

A theory is proposed to account for unawareness of blindness, hemianopsia, and hemiplegia, and for phantom limb after amputation. It is assumed that interruption of a sensory pathway at any level--from peripheral nerve to primary sensory cortex--is not associated with any immediate sensory experience that uniquely specifies the defect. Instead the sensory loss must be discovered by a process of self-observation and inference. Discovery is easy for defects that create major functional disability, such as total blindness. Hence unawareness of total blindness occurs only in association with severe intellectual impairment, precluding the required self-observation and inference. In contrast, hemianopsia is difficult to discover because several mechanisms automatically compensate the defect effectively. Thus unawareness of hemianopsia is common, even in intellectually normal individuals. Insensate fields are often the source of suggested (false) percepts, because no information from such a field specifies the absence of a sensory stimulus. The most powerful source of suggestion is sensory activity in uninvolved portions of the affected sensory field. Thus hemianopsics may perceive complete geometric forms when only incomplete forms are shown and the missing portion falls in the hemianopsic fields. Such perceptual completion also occurs in hemianesthetic hemiplegics, creating the illusion that there are normally functioning limbs on the affected side. This perceptual completion increases the difficulty of discovery of hemianesthetic hemiplegia, but the disability is still sufficiently obvious that some additional cognitive impairment is invariably present in patients with lasting unawareness of hemiplegia. Phantom limb after amputation is the product of perceptual completion without associated cognitive impairment. The patient with phantom limb is thus aware of the illusory quality of his phantom. Some insight into the neural basis of perceptual completion and of unawareness of sensory loss may derive from considering sensory systems and associative cortex as parallel-distributed processing mechanisms.

Adult↗
PubMed1989

Prosopagnosia: a defect in visual configural processing.

A patient with severe, lasting prosopagnosia could not get an immediate overview of a face sufficiently specific for successful identification. He also failed completely in tasks of visual closure despite adequate performances on numerous other tests of visual perception and memory. We conclude that prosopagnosia represents a loss of visual "configural processing"--a learned skill enabling immediate identification of individual members of a class without conscious visuospatial analysis or remembering. Prosopagnosia and agnosic alexia represent two distinct defects of configural processing: Alexics cannot identify items with distinctive features that are themselves identifiable. Prosopagnosics cannot identify objects whose critical distinguishing features have no independent identities.

Adult↗
PubMed1988

Crossed buccofacial apraxia.

The cerebral hemisphere contralateral to the preferred hand is generally dominant for learned representational motor acts, including those involving buccofacial muscles. It is generally also language-dominant. This buccofacial apraxia has, with rare exceptions, been associated with left hemispheric lesions in right-handers. We describe two patients with severe buccofacial apraxia caused by large middle cerebral artery territory infarcts in the hemisphere ipsilateral to the preferred hand and nondominant for language. Neither patient had aphasia or major limb apraxia. Computed tomographic scans in the first patient and neuropathologic examination in the second failed to reveal an abnormality of the hemisphere contralateral to the preferred hand. Hence, in some individuals, the hemisphere controlling skilled representational buccofacial movements may not be the one that is dominant either for handedness or for language.

Aged↗
PubMed1988

Pure agraphia and Gerstmann's syndrome as a visuospatial-language dissociation: an experimental case study.

A right-handed man suffered a left parieto-occipital cerebral infarction, causing agraphia with Gerstmann's syndrome but without major aphasia, alexia, or apraxia. Oral spelling was superior to written spelling. Experiments were performed involving (1) analysis of errors in writing, (2) tasks of visual imagery, and (3) identifying letters drawn without leaving a visual trace. The results suggest that the agraphia and Gerstmann's syndrome are due to a dissociation of language skills and visuospatial skills caused by a dominant parieto-occipital lesion.

Aged↗
PubMed1988

A case study of mental imagery deficit.

We describe a patient with a deficit in imagery ability, following a left posterior cerebral artery infarction and possible anoxic episode. This deficit was inferred from the patient's performance on several tasks, including one in which normal adults are known to rely on imagery and two that tested imagery nonverbally, allowing us to examine the possibility of a language-imagery disconnection. In addition, we queried the patient on some cognitive capacities related to visual imagery: dreaming, geographical knowledge, and introspection regarding visual and auditory imagery. Hypotheses concerning the critical lesion site and underlying cognitive mechanism of image generation deficits are discussed in relation to this and other recent cases of impaired imagery ability with intact recognition ability, and the relevance of this deficit to the "imagery debate" is discussed.

Anomia↗
PubMed1987

Left visual spatial neglect is both environment-centered and body-centered.

To determine whether the left space that is neglected after right hemisphere lesions is body centered or environment centered, we asked patients with right hemisphere stroke and normal controls to report the contents of spatial arrays of objects or words, either while seated or while reclining on their side. The reclining posture eliminated the alignment of the vertical axis of the body with the vertical axis of the environment. Patients made fewer reports to the body left, but also fewer reports to the environment left, independent of body position. This suggest that a cerebral hemisphere directs attention not only relative to the body midline axis, but also relative to an environmental reference frame.

Aged↗