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Vascular dementia is dementia caused by a series of strokes. Restricted blood flow due to strokes reduces oxygen and glucose delivery to the brain, causing cell injury and neurological deficits in the affected region. Subtypes of vascular dementia include subcortical vascular dementia, multi-infarct dementia, stroke-related dementia, and mixed dementia.
The caudate nucleus is one of the structures that make up the corpus striatum, which is part of the basal ganglia in the human brain. Although the caudate nucleus has long been associated with motor processes because of its role in Parkinson's disease, it also plays important roles in nonmotor functions, such as procedural learning, associative learning, and inhibitory control of action. The caudate is also one of the brain structures that compose the reward system, and it functions as part of the cortico-basal ganglia-thalamo-cortical loop.
Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical condition. Anosognosia results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, the term was first coined by the neurologist Joseph Babinski in 1914, in order to describe the unawareness of hemiplegia.
Cerebral atrophy is a common feature of many of the diseases that affect the brain. 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. Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location. If the cerebral hemispheres are affected, conscious thought and voluntary processes may be impaired.
Frontotemporal lobar degeneration (FTLD) is a pathological process that occurs in frontotemporal dementia. It is characterized by atrophy in the frontal lobe and temporal lobe of the brain, with sparing of the parietal and occipital lobes.
Cerebral amyloid angiopathy (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to medium blood vessels of the central nervous system and meninges. The term congophilic is sometimes used because the presence of the abnormal aggregations of amyloid can be demonstrated by microscopic examination of brain tissue after staining with Congo red. The amyloid material is only found in the brain and as such the disease is not related to other forms of amyloidosis.
Neurofibrillary tangles (NFTs) are intracellular aggregates of hyperphosphorylated tau protein that are most commonly known as a primary biomarker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies. Little is known about their exact relationship to the different pathologies.
A perivascular space, also known as a Virchow–Robin space, is a fluid-filled space surrounding certain blood vessels in several organs, including the brain, potentially having an immunological function, but more broadly a dispersive role for neural and blood-derived messengers. The brain pia mater is reflected from the surface of the brain onto the surface of blood vessels in the subarachnoid space. In the brain, perivascular cuffs are regions of leukocyte aggregation in the perivascular spaces, usually found in patients with viral encephalitis.
Arteriolosclerosis is a form of cardiovascular disease involving hardening and loss of elasticity of arterioles or small arteries and is most often associated with hypertension and diabetes mellitus. Types include hyaline arteriolosclerosis and hyperplastic arteriolosclerosis, both involved with vessel wall thickening and luminal narrowing that may cause downstream ischemic injury. The following two terms whilst similar, are distinct in both spelling and meaning and may easily be confused with arteriolosclerosis.
HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. It is a syndrome of progressive deterioration of memory, cognition, behavior, and motor function in HIV-infected individuals during the late stages of the disease, when immunodeficiency is severe. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of HIV-associated dementia (HAD) are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.
Lacunar stroke or lacunar cerebral infarct (LACI) is the most common type of ischemic stroke, resulting from the occlusion of small penetrating arteries that provide blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as having lacunar stroke syndrome (LACS).
The retrosplenial cortex (RSC) is a cortical area in the brain comprising Brodmann areas 29 and 30. It is secondary association cortex, making connections with numerous other brain regions. The region's name refers to its anatomical location immediately behind the splenium of the corpus callosum in primates, although in rodents it is located more towards the brain surface and is relatively larger. Its function is currently not well understood, but its location close to visual areas and also to the hippocampal spatial/memory system suggest it may have a role in mediating between perceptual and memory functions, particularly in the spatial domain. However, its exact contribution to either space or memory processing has been hard to pin down.
Posterior cortical atrophy (PCA), also called Benson's syndrome, is a rare form of dementia which is considered a visual variant or an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.
Lipohyalinosis is a cerebral small vessel disease affecting the small arteries, arterioles or capillaries in the brain. Originally defined by C. Miller Fisher as 'segmental arteriolar wall disorganisation', it is characterized by vessel wall thickening and a resultant reduction in luminal diameter. Fisher considered this small vessel disease to be the result of hypertension, induced in the acute stage by fibrinoid necrosis that would lead to occlusion and hence lacunar stroke. However, recent evidence suggests that endothelial dysfunction as a result of inflammation is a more likely cause for it. This may occur subsequent to blood–brain barrier failure, and lead to extravasation of serum components into the brain that are potentially toxic. Lacunar infarction could thus occur in this way, and the narrowing – the hallmark feature of lipohyalinosis – may merely be a feature of the swelling occurring around it that squeezes on the structure.
Alzheimer's disease (AD) is a neurodegenerative disease that usually starts slowly and progressively worsens. It is the cause of 60–70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. As the disease advances, symptoms can include problems with language, disorientation, mood swings, loss of motivation, self-neglect, and behavioral issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to twelve years.
A hyperintensity or T2 hyperintensity is an area of high intensity on types of magnetic resonance imaging (MRI) scans of the brain of a human or of another mammal that reflect lesions produced largely by demyelination and axonal loss. These small regions of high intensity are observed on T2 weighted MRI images within cerebral white matter or subcortical gray matter. The volume and frequency is strongly associated with increasing age. They are also seen in a number of neurological disorders and psychiatric illnesses. For example, deep white matter hyperintensities are 2.5 to 3 times more likely to occur in bipolar disorder and major depressive disorder than control subjects. WMH volume, calculated as a potential diagnostic measure, has been shown to correlate to certain cognitive factors. Hyperintensities appear as "bright signals" on an MRI image and the term "bright signal" is occasionally used as a synonym for a hyperintensity.
Subcortical dementias includes those diseases which predominantly affects the basal ganglia along with features of cognitive decline.
LATE is a term that describes a prevalent medical condition with impaired memory and thinking in advanced age, often culminating in the dementia clinical syndrome. In other words, the symptoms of LATE are similar to those of Alzheimer's disease.
Hypertension is a condition characterized by an elevated blood pressure in which the long term consequences include cardiovascular disease, kidney disease, adrenal gland tumors, vision impairment, memory loss, metabolic syndrome, stroke and dementia. It affects nearly 1 in 2 Americans and remains as a contributing cause of death in the United States. There are many genetic and environmental factors involved with the development of hypertension including genetics, diet, and stress.
The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons. The NVU addresses the brain's unique dilemma of having high energy demands yet low energy storage capacity. In order to function properly, the brain must receive substrates for energy metabolism–mainly glucose–in specific areas, quantities, and times. Neurons do not have the same ability as, for example, muscle cells, which can use up their energy reserves and refill them later; therefore, cerebral metabolism must be driven in the moment. The neurovascular unit facilitates this ad hoc delivery and, thus, ensures that neuronal activity can continue seamlessly.
References
- ↑ Kalaria, J. Attems. "Microinfarction". www.sciencedirect.com/. Retrieved 15 October 2021.
- ↑ Shih, Andy Y.; Blinder, Pablo; Tsai, Philbert S.; Friedman, Beth; Stanley, Geoffrey; Lyden, Patrick D. (2013). "The smallest stroke: Occlusion of one penetrating vessel leads to infarction and a cognitive deficit". Nature Neuroscience. 16 (1). National Institute of Health: 55–63. doi:10.1038/nn.3278. PMC 3952571 . PMID 23242312 . Retrieved 15 October 2021.
- ↑ Microinfarcts – Small Size, Big Impact Archived 2014-09-01 at archive.today . Hotchkiss Brain Institute. Retrieved September 1, 2014
- ↑ Smith, Eric E.; Schneider, Julie A.; Wardlaw, Joanna M.; Greenberg, Steven M. (2012). "Cerebral Microinfarcts: The Invisible Lesions". The Lancet. Neurology. 11 (3). National Institute of Health: 272–282. doi:10.1016/S1474-4422(11)70307-6. PMC 3359329 . PMID 22341035 . Retrieved 15 October 2021.
- 1 2 3 4 Smith, Eric E. MD, Julie A. Schneider, MD, Joanna M. Wardlaw, MD, and Steven M. Greenberg, MD. “Cerebral Microinfarcts: The Invisible Lesions.” Lancet Neurology 11.3 (2012): 272–282. PMC. Web. 20 Mar. 2016.
- ↑ Wang M, Iliff JJ, Liao Y, Chen MJ, Shinseki MS, Venkataraman A, Cheung J, Wang W, Nedergaard M. Cognitive deficits and delayed neuronal loss in a mouse model of multiple microinfarcts. J Neurosci PubMed.
- 1 2 Kövari, Enikö, MD, Gabriel Gold, MD, François R. Herrmann, MD, MPH, Alessandra Canuto, MD, Patrick R. Hof, MD, Jean-Pierre Michel, MD, Constantin Bouras, MD, and Panteleimon Giannakopoulos, MD. "Cortical Microinfarcts and Demyelination Significantly Affect Cognition in Brain Aging." Stroke 35 (2004): 410-14. Ahajournals.org Web. 20 Mar. 2016.
- 1 2 Arvanitakis, Zoe; Leurgans, Sue E.; Barnes, Lisa L.; Bennett, David A.; Schneider, Julie A. (March 2011). "Microinfarct Pathology, Dementia, and Cognitive Systems". Stroke. 42 (3): 722–727. doi:10.1161/strokeaha.110.595082. PMC 3042494 . PMID 21212395.