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Cerebral atrophy

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Cerebral atrophy is a common feature of many of the diseases that affect the brain.[1] Atrophy of any tissue means a decrement in the size of the cell, which can be due to progressive loss of cytoplasmic proteins. In brain tissue, atrophy describes a loss of neurons and the connections between them. Brain atrophy can be classified into two main categories: generalized and focal atrophy.[2] Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location.[2] If the cerebral hemispheres (the two lobes of the brain that form the cerebrum) are affected, conscious thought and voluntary processes may be impaired.

Symptoms

Difficulty standing upright

-Loss of coordination.

-Partial paralysis.

-Absence of physical sensation in certain parts of the body.

-Double or unfocused vision.

-Difficulties speaking or understanding speech (aphasia).

Causes

Diseases and disorders

Pick's disease showing brain atrophy

Infections

include...

  • brain
  • chord

Drug-induced

Diagnosis

Neurofilament light chain

Main article: Neurofilament light chain

Measures

Brain CT with different grading systems of cerebral atrophy (seen as decreased size of gyri and secondary increased size of sulci):[7]
- Medial temporal lobe atrophy (MTA)
- Posterior atrophy (PA)
- Frontal cortical atrophy (fGCA)

CT and MRI are most commonly used to observe the brain for cerebral atrophy. A CT scan takes cross sectional images of the brain using X-rays, while an MRI uses a magnetic field. With both measures, multiple images can be compared to see if there is a loss in brain volume over time.[8]

Difference from hydrocephalus

Cerebral atrophy can be hard to distinguish from hydrocephalus because both cerebral atrophy and hydrocephalus involve an increase in cerebrospinal fluid (CSF) volume. In cerebral atrophy, this increase in CSF volume comes as a result of the decrease in cortical volume. In hydrocephalus, the increase in volume happens due to the CSF itself.[8]

Typical imaging findings in normal pressure hydrocephalus versus brain atrophy.[9]
Normal pressure hydrocephalus Brain atrophy
Preferable projection Coronal plane at the level of the posterior commissure of the brain.
Modality in this example CT MRI
CSF spaces over the convexity near the vertex (red ellipse ) Narrowed convexity ("tight convexity") as well as medial cisterns Widened vertex (red arrow) and medial cisterns (green arrow)
Callosal angle (blue V) Acute angle Obtuse angle
Most likely cause of leucoaraiosis (periventricular signal alterations, blue arrows ) Transependymal cerebrospinal fluid diapedesis Vascular encephalopathy, in this case suggested by unilateral occurrence

Treatment

Cerebral atrophy is not usually preventable. However, there are steps that can be taken to reduce the risk:

  • controlling blood pressure
  • a healthy balanced diet including omega-3's and antioxidants
  • staying active mentally, physically, and socially.[10]

Reversibility of cerebral atrophy

While most cerebral atrophy is said to be irreversible, recent studies that show this is not always the case. A child who was treated with ACTH originally showed atrophy, but four months after treatment the brain was seemingly normal again.[11]

As previously mentioned, chronic alcoholism is known to be associated with significant brain damage.[12] The pronounced shrinkage in the frontal lobes and cerebellum of alcoholics correlates with serious impairments in executive and psychomotor functions. However, longitudinal studies suggest that some of these brain damages are partially reversible with abstinence[6]. In response to drinking cessation, bodies of gray and white matter including the cerebral cortex, the limbic system (amygdala, hippocampus, thalamus), the cerebellum, and the brainstem all showed a general increase in brain volume.[13] Similarly, ventricular enlargement—which reflects atrophy of surrounding brain regions—is also reduced in abstinent alcoholics. Following extended sobriety, the volume of the lateral and third ventricles was decreased, and abstainers showed an improvement in working memory and balance.[6] Finally, evidence for the recovery of brain volume with continued sobriety is supported by the improvement in neuropsychological performance. Compared to the control participants, abstinent alcoholic patients scored significantly better on tests measuring cognitive, sensory, and motor functions including abstract reasoning, memory, visuospatial ability, and gait and balance.[6] That being said, while short-term abstinence suffices to produce structural and functional recovery, some alcohol-induced brain changes may persist even after long-term sobriety.[6]

See also

References

  1. ^ "Cerebral Atrophy Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". Archived from the original on 2016-03-04. Retrieved 2014-03-28.
  2. ^ a b Harris TC, de Rooij R, Kuhl E (September 2019). "The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury". Annals of Biomedical Engineering. 47 (9): 1941–1959. doi:10.1007/s10439-018-02148-2. PMC 6757025. PMID 30341741.
  3. ^ Harris, Taylor C.; de Rooij, Rijk; Kuhl, Ellen (2018-10-17). "The Shrinking Brain: Cerebral Atrophy Following Traumatic Brain Injury". Annals of Biomedical Engineering. 47 (9). Springer Science and Business Media LLC: 1941–1959. doi:10.1007/s10439-018-02148-2. ISSN 0090-6964. PMC 6757025. PMID 30341741.
  4. ^ Fox NC, Schott JM (January 2004). "Imaging cerebral atrophy: normal ageing to Alzheimer's disease". Lancet. 363 (9406): 392–394. doi:10.1016/S0140-6736(04)15441-X. PMID 15074306. S2CID 20494612.
  5. ^ Andreasen NC, Liu D, Ziebell S, Vora A, Ho BC (June 2013). "Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study". The American Journal of Psychiatry. 170 (6): 609–615. doi:10.1176/appi.ajp.2013.12050674. PMC 3835590. PMID 23558429.
  6. ^ a b c d e Rosenbloom MJ, Pfefferbaum A (2008). "Magnetic resonance imaging of the living brain: evidence for brain degeneration among alcoholics and recovery with abstinence". Alcohol Research & Health. 31 (4): 362–376. PMC 3860463. PMID 23584010.
  7. ^ Velickaite V, Giedraitis V, Ström K, Alafuzoff I, Zetterberg H, Lannfelt L, et al. (September 2017). "Cognitive function in very old men does not correlate to biomarkers of Alzheimer's disease". BMC Geriatrics. 17 (1): 208. doi:10.1186/s12877-017-0601-6. PMC 5591537. PMID 28886705.{{cite journal}}: CS1 maint: unflagged free DOI (link) Creative Commons Attribution 4.0 International License
  8. ^ a b "Cerebral Atrophy".
  9. ^ Damasceno BP (2015). "Neuroimaging in normal pressure hydrocephalus". Dementia & Neuropsychologia. 9 (4): 350–355. doi:10.1590/1980-57642015DN94000350. PMC 5619317. PMID 29213984.
  10. ^ "Cerebral Atrophy: Causes". Archived from the original on 26 January 2015. Retrieved 26 January 2015.
  11. ^ Gordon N (August 1980). "Apparent cerebral atrophy in patients on treatment with steroids". Developmental Medicine and Child Neurology. 22 (4): 502–506. doi:10.1111/j.1469-8749.1980.tb04355.x. PMID 6250932. S2CID 32099986.
  12. ^ Meyer JS, Quenzer LF (2013). Psychopharmacology: Drugs, The Brain, and Behavior (2nd ed.). Sinauer Associates.
  13. ^ Zahr NM, Pfefferbaum A (2017). "Alcohol's Effects on the Brain: Neuroimaging Results in Humans and Animal Models". Alcohol Research. 38 (2): 183–206. PMC 5513685. PMID 28988573.
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