Neurological problems can be quite intimidating for adults and children alike, and it is crucial to start treatment as early as possible. It is study of neurological care for both adults and children. It includes examination, testing, diagnosis and treatment of the patient. Brain Mapping is set of neuroscience techniques predicated on the mapping of biological quantities or properties onto spatial representations of the human brain resulting in maps. Brain mapping is further defined as the study of the anatomy and function of the brain and spinal cord through the use of imaging including intra-operative, microscopic, endoscopic and multi-modality imaging.
In this we can study Brain and other elements of the nervous system. The brain is the most complex part of the human body. This three-pound organ is the seat of intelligence, interpreter of the senses, initiator of body movement, and controller of behavior. This gives us basic information about the human brain. It may help us to understand how the healthy brain works, how to keep it healthy, and what happens when the brain is diseased or dysfunctional.
An overview of the relevant aspects of the epidemiology, clinical presentation, basic disease mechanisms, diagnostic approaches and treatment options of the most common neurological diseases.
This course will provide a basic overview of the most common and important neurological diseases and conditions affecting people worldwide: stroke, epilepsy, headache, back pain, neurodegenerative diseases , movement disorders, alterations of consciousness, nervous system infections, traumatic brain injury, and neuromuscular diseases. Clinical Neurosurgery is the medical specialty concerned with the prevention, diagnosis, treatment, and rehabilitation of disorders which affect any portion of the nervous system including the brain, spinal cord, peripheral nerves, and extra-cranial cerebrovascular system.
It is known as progressive loss of structure or function of neurons, including death of neurons. The diseases due to Neurodegeneration are incurable and often strike older adults and are characterized by progressive deterioration of nerve cells, eventually leading to cell death. A focal neurologic deficit consists of a set of symptoms or signs in which causation can be localized to an anatomic site in the central nervous system. The sudden development of a focal neurologic deficit suggests a vascular ischemic event such as an infarction.
Chronically worsening focal neurologic deficits may be caused by an expanding intracranial lesion such as a primary or metastatic neoplasm. All Published work is licensed under a Creative Commons Attribution 4. About Journal of Neurology and Neuroscience. Recent Articles. Journal Highlights. Tweets by NeurologyNeuros.
Professor Jason Warren | Dementia Research Centre - UCL - London's Global University
Further, the delay interval did not significantly differ across the 3 groups; the mean SD was Words and shapes were evaluated for accuracy and placement using scoring criteria that have been described previously. Full credit was given for recognition scores in cases where delayed recall scores were perfect. All patients in the present study were required to score within 1.
Owing to the retrospective nature of the study, patients differed in the amount and type of clinical and neuropsychological assessments available from the time of 3W3S test administration. Fourteen of 19 patients Functional impairment was used to estimate disease severity in the present study because in a longitudinal study 25 of patients with PPA, ADLQ scores declined far less dramatically than did Mini-Mental State Examination scores, suggesting that the true level of clinical severity in PPA may be overestimated by the Mini-Mental State Examination or other assessments that contain a high proportion of verbal items.
In cases where the 3 groups differed significantly from one another, post hoc t tests were used to identify significant pairwise differences. For all patients, the mean SD age was Seventeen of 19 patients Eight patients demonstrated a significant naming impairment on the BNT.
Of note, these 8 patients all obtained perfect word acquisition scores, suggesting that even those with the most severe naming deficits were capable of learning and producing the words on the 3W3S test. The interval between 3W3S test administration and death did not significantly differ across the 3 groups; the mean SD age was 8.
All patients with PPA-FTLD in the sample were diagnosed with a variant of tau pathology: 2 were diagnosed as having corticobasal degeneration, 1 as having progressive supranuclear palsy, and 3 as having Pick disease. None of the patients showed evidence of Lewy-type synuclein pathology. Additional details on the clinical and neuropathologic features of all 13 patients with PPA were reported in 2 prior autopsy studies, 4 , 5 and additional details on 4 of the patients with PPA-AD and 3 with AMN-AD were reported in an additional autopsy study.
This difference was a function of neuropathologic, rather than clinical, diagnosis. To identify within-group differences in effortless learning, incidental recall was compared with the copy condition in each group. This difference was also a function of neuropathologic, rather than clinical, diagnosis. To identify within-group differences in the capacity for retrieval of previously learned material, delayed recall was compared with acquisition in each group.
This difference was a function of clinical, rather than neuropathologic, diagnosis. To identify within-group differences in retention, recognition was compared with delayed recall in each group. This finding is inconsistent with the results of clinical studies that report verbal but not nonverbal memory deficits in patients with PPA. Furthermore, the 3W3S test is delivered entirely in the visual modality, whereas standard verbal memory tests typically occur in the auditory modality while nonverbal memory is tested through drawing.
The present study aimed to identify differences in episodic memory performance as a function of neuropathologic and clinical diagnoses in an autopsy-confirmed series of patients with dementia. The instrument that we used, the 3W3S test, was designed to identify differences in verbal and nonverbal learning and memory within each diagnostic group.
As hypothesized, performance on portions of the 3W3S test that measure effortless learning, delayed retrieval, and retention distinguished among the 3 diagnostic groups of similar demographic composition and clinical severity. Those with clinically amnestic dementia also showed a deficit in nonverbal effortless learning, which was not observed in either PPA group.
Retention, the aspect of learning and memory most closely linked to episodic memory and its limbic substrate, 30 was impaired only in the AMN-AD group. In most cases, Alzheimer pathology selectively accumulates in medial temporal regions critical for memory, leading to an initially primary amnestic syndrome. Future research on the association of these deficits to the distribution of pathology could provide valuable information on interactions between limbic and language networks.
Our findings provide support for the 3W3S test as a practical and informative test of episodic memory in patients with dementia. It is brief and easy to administer and interpret in outpatient clinical settings. In patients with suspected PPA, the 3W3S test may actually prove more useful than standard memory tests, given that it was designed to minimize extraneous language demands and to compare subtle verbal and nonverbal features of memory.
Limitations of the present study must be addressed. Namely, the small sample size may have limited the power to detect some differences, like material specificity, previously reported in studies of memory in patients with PPA. Detailed clinical and neuropsychological data were not uniformly collected from all patients at the time of the 3W3S test administration.
Six patients did not have a formal ADLQ rating available, so clinical severity had to be qualitatively rated based on medical record review of historical information. The present study helped to characterize differential patterns of verbal and nonverbal learning and memory in relation to neuropathology in autopsy-confirmed cases of PPA. Our findings are consistent with our previous study 12 and other reports 28 that retentive memory is largely preserved in all cases of clinical PPA.
However, our study also shows that patients with PPA with Alzheimer pathology have selective vulnerabilities in effortless learning and delayed retrieval of verbal information, whereas patients with PPA—FTLD-tau neuropathology do not. Published Online: May 16, Author Contributions: Ms Kielb had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Critical revision of the manuscript for important intellectual content: Kielb, Wieneke, Bigio, Mesulam, Rogalski, Weintraub. Ms Shaw was not compensated for her contribution. All Rights Reserved. View Large Download. Demographic and Clinical Characteristics by Group. Primary progressive aphasia. Ann Neurol. PubMed Google Scholar Crossref.
Classification of primary progressive aphasia and its variants. Primary progressive aphasia and kindred disorders.
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