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In the cerebrum and cerebellum, white matter is predominantly found in deeper areas — with gray matter coating the white matter - see figure 1. Other gray matter structures, like the basal ganglia, are embedded within this white matter core. Figure 2: The arrangement of white and gray matter in the spinal cord. The white fatty myelin that gives this tissue its name is also essential to its function — myelin insulates axons, letting the signal within travel far faster, enabling the nerve cell function that is essential to normal motor and sensory function.
Leave a Comment. Spinal cord injuries are traumatic for patients and their families. They cause disruptive changes to every aspect of your life and there is a lot of new information to navigate and understand. Our experts have collected everything in one place to help you learn more about your injury, locate doctors and treatment centers, find financial support, and get assistance navigating your next move.
Grey Matter in the Brain and Spinal Cord Gray matter, named for its pinkish-gray color, is home to neural cell bodies, axon terminals, and dendrites, as well as all nerve synapses. White Matter in the Brain and Spinal Cord The white matter of your brain and spinal cord is composed of bundles of axons. White Matter, Grey Matter, and Spinal Tracts Together, the gray and white matter of your brain and spinal cord help form spinal tracts.
Those tracts include: Posterior tracts : These tracts, located at the back of your spinal cord, convey information from your skin about pressure, touch, and pain.
They also help you position your body and space, so you can move according to your surroundings. Spinothalamic tracts: These sensory tracts tell your brain about your body's temperature and pain level. Corticospinal tracts: These motor tracts send nerve signals from the brain, down the spinal cord, and into various skeletal muscles, enabling you to move.
Topics: Traumatic Brain Injury. As medical and surgical treatments for white matter disorders improve, opportunities for effective early intervention do also. Exciting possibilities are on the horizon for many white matter disorders using gene therapy and stem cells. Potentially, stimulants and cholinesterase inhibitors will counteract the slowing of attention and memory loss. But much clinical experience supports the sense that cognitive dysfunction is prevalent among these white matter disorders.
Moreover, research suggests that syndromes of widespread white matter dysfunction far outnumber syndromes of isolated, regional white matter dysfunction. Similarly, although neuropsychiatric syndromes such as depression are common in patients with white matter disorders, they may result from many causes, so the cause-effect relationship is less clear. All this suggests that cognitive impairment will prove to be a leading source of clinical distress and disability in cases of damage to cerebral white matter.
Not surprisingly, in early stages of any white matter disorder milder cognitive dysfunction is more common than dementia, but dementia often follows. In MS, for example, estimates are that 10 to 20 percent of patients will develop dementia.
Despite this, it is important to realize that in clinical practice the recognition of early cognitive dysfunction in the white matter disorders is far from simple. Many patients show subtle cognitive symptoms and signs, frequently co-mingled with other neurologic or medical features of their disease, challenging the clinician to interpret the relationship of white matter manifestations to cognitive status.
Moreover, the range of clinical features that herald the onset of cerebral white matter involvement is impressively broad: inattention, executive dysfunction, confusion, memory loss, personality change, depression, somnolence, lassitude, and fatigue.
How do cognitive dysfunction and dementia actually present themselves to the physician? In terms of brain anatomy, sustained attention concentration, vigilance , executive thinking, and memory retrieval are all closely associated with the operation of the frontal lobes, and most white matter disorders show a preference for the frontal white matter. Even when white matter lesions are situated in more posterior cerebral locations, frontal lobe functions are still affected, probably because of the dense connectivity between frontal and other regions.
Visuospatial skills are also affected in white matter disorders. In contrast, language is typically normal or only mildly affected in patients with white matter disorders because the language-related cortex is spared. Motor function also tends to be intact, in keeping with the relative sparing of deep gray matter structures. Likewise, procedural memory, or memory for skills such as bicycle riding, is retained.
What about white matter lesions linked with narrower brain-behavior disturbances, including classic syndromes such as aphasia and amnesia? Although these are rightly viewed as more common with cortical lesions, recent research also links them with white matter damage. For example, there are reports of isolated amnesia associated with stroke that affects a white matter region called the mamillothalamic tract. A language disturbance known as conduction aphasia is related to MS plaque in another part of the brain, the left arcuate fasciculus.
Thus, although they are uncommon compared with syndromes caused by diffuse white matter damage, the focal brain-behavior syndromes illustrate the importance of white matter tracts in all domains of higher function. Research here can enhance our understanding of the neural networks that underlie these higher brain functions.
Abnormalities of cerebral white matter are associated with a spectrum of emotional disturbances. This category of disorders is vaguer than the brain-behavior syndromes because the correlation of white matter disorders with psychiatric syndromes is much less clear; and psychiatric impairments are notorious for having multiple causes.
Still, there is much new information on the role of white matter in emotional function, shedding light on both white matter disorders and psychiatric diseases. These neuropsychiatric syndromes fall into two general groups: psychiatric features in patients who have known white-matter disorders, and the many psychiatric diseases in which white matter abnormalities are implicated.
In patients with known white matter disorders, reports document the presence of depression, mania, psychosis, pathologic crying or laughing, and euphoria. We do not know, as yet, how closely these psychiatric syndromes correlate with measures of white matter dysfunction. When it comes to primary psychiatric diseases, often considered idiopathic of uncertain cause and as yet not linked with structural brain damage, there are recent intriguing reports from neuroimaging research on the structure of white matter.
In patients with schizophrenia, for example, imaging studies have detected microscopic abnormalities in white matter structures, and widespread myelin and oligodendrocyte dysfunction are linked with altered cerebral connectivity.
MRI studies have found that white matter abnormalities are more common in patients with bipolar disorder than in the general population. In contrast, an increase in the volume of hemispheric white matter in all lobes was observed in autism. Finally, diffusion tensor imaging studies of schizophrenic men found a correlation of inferior frontal lobe white matter abnormalities with impulsive aggression.
Obviously, we need far more detailed investigation of how white matter abnormalities may contribute to psychiatric disease, perhaps by disrupting neural networks devoted to emotional function.
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