This document discusses hereditary spastic paraplegia (HSP), a genetic disorder characterized by progressive stiffening and weakness of the lower limbs. HSP is caused by degeneration of motor nerve fibers in the spinal cord that control the lower limbs. Over 40 genes have been associated with HSP, which can be inherited in autosomal dominant, recessive, or X-linked patterns. Symptoms include spasticity, weakness, and abnormal gait in the lower limbs. Treatment focuses on managing symptoms through medications, physical therapy, and assistive devices. Genetic testing can confirm a diagnosis of HSP but over 40% of cases do not have an identified genetic cause.
The document provides an overview of the basal ganglia. It discusses the physiological anatomy and components of the basal ganglia, including the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. It describes the connections and functional neuronal circuits of the basal ganglia. The functions of the basal ganglia in motor control and disorders such as Parkinson's disease, chorea, athetosis, and Huntington's disease are summarized.
Extrapyramidal symptoms. ... These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (motor restlessness), parkinsonism (characteristic symptoms such as rigidity), bradykinesia (slowness of movement), and tremor, and tardive dyskinesia (irregular, jerky movements).
A 4 month old baby presented with infantile spasms. The EEG showed a hypsarrhythmic background pattern with high amplitude, poorly organized brain waves. An asynchronous slow wave correlated with the baby's clinical spasm. This is consistent with West syndrome, which is characterized by the triad of infantile spasms, arrest of psychomotor development, and hypsarrhythmia on EEG.
The document discusses epileptic encephalopathy syndromes that occur in neonates, infants, and children. It describes the key features of early myoclonic encephalopathy, West syndrome, Lennox-Gastaut syndrome, Landau-Kleffner syndrome, and continuous spike-wave during sleep. The syndromes are characterized by seizures, developmental regression or impairment, and specific electrographic findings on EEG. Prognosis varies between syndromes but is often poor, with cognitive and neurological deficits. Treatment involves antiepileptic drugs, corticosteroids, ketogenic diet, or surgery in refractory cases.
This document summarizes different types of generalized epilepsies based on their EEG patterns and clinical presentations. It discusses primary generalized epilepsies, which have no identifiable cause and normal brain imaging. It also discusses more serious secondary generalized epilepsies, which are caused by diffuse brain injury and often associated with developmental delays. Specific syndromes like Lennox-Gastaut syndrome and West syndrome are examined in detail based on their characteristic EEG patterns including slow spike wave discharges, hypsarrhythmia, and independent multifocal spike discharges.
The document provides an overview of the basal ganglia. It discusses the physiological anatomy and components of the basal ganglia, including the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. It describes the connections and functional neuronal circuits of the basal ganglia. The functions of the basal ganglia in motor control and disorders such as Parkinson's disease, chorea, athetosis, and Huntington's disease are summarized.
Extrapyramidal symptoms. ... These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (motor restlessness), parkinsonism (characteristic symptoms such as rigidity), bradykinesia (slowness of movement), and tremor, and tardive dyskinesia (irregular, jerky movements).
A 4 month old baby presented with infantile spasms. The EEG showed a hypsarrhythmic background pattern with high amplitude, poorly organized brain waves. An asynchronous slow wave correlated with the baby's clinical spasm. This is consistent with West syndrome, which is characterized by the triad of infantile spasms, arrest of psychomotor development, and hypsarrhythmia on EEG.
The document discusses epileptic encephalopathy syndromes that occur in neonates, infants, and children. It describes the key features of early myoclonic encephalopathy, West syndrome, Lennox-Gastaut syndrome, Landau-Kleffner syndrome, and continuous spike-wave during sleep. The syndromes are characterized by seizures, developmental regression or impairment, and specific electrographic findings on EEG. Prognosis varies between syndromes but is often poor, with cognitive and neurological deficits. Treatment involves antiepileptic drugs, corticosteroids, ketogenic diet, or surgery in refractory cases.
This document summarizes different types of generalized epilepsies based on their EEG patterns and clinical presentations. It discusses primary generalized epilepsies, which have no identifiable cause and normal brain imaging. It also discusses more serious secondary generalized epilepsies, which are caused by diffuse brain injury and often associated with developmental delays. Specific syndromes like Lennox-Gastaut syndrome and West syndrome are examined in detail based on their characteristic EEG patterns including slow spike wave discharges, hypsarrhythmia, and independent multifocal spike discharges.
Temporal lobe epilepsy is one of the most common forms of epilepsy. It can be caused by hippocampal sclerosis or lesions in the temporal lobe. Hippocampal sclerosis involves neuronal loss and gliosis in the hippocampus and is the most common pathological finding in temporal lobe epilepsy patients. Interictal EEG findings like temporal intermittent rhythmic delta activity and temporal sharp waves help lateralize the seizure focus. Video EEG monitoring helps capture seizures and interictal discharges. Treatment involves antiepileptic drugs and potentially resective surgery for drug-resistant cases.
Partial complex epilepsy is characterized by focal seizures that impair consciousness. It is most commonly caused by temporal lobe epilepsy but can arise from other brain regions. Diagnosis involves obtaining a detailed history, physical exam, EEG, and MRI brain imaging. Treatment includes antiepileptic medications and potentially surgery for drug-resistant cases. Surgical options include temporal lobectomy for temporal lobe epilepsy, which can cure seizures in over 50% of carefully selected patients. Prognosis depends on seizure frequency and underlying etiology.
Extrapyramidal System and Disorders of Extrapyramidal SystemChetan Ganteppanavar
The document discusses the extrapyramidal system and disorders of the extrapyramidal system. It begins by defining the extrapyramidal system as referring to the basal ganglia and array of brainstem nuclei. It then lists the components and tracts of the extrapyramidal system. The document goes on to discuss disorders like Parkinson's disease, classifying extrapyramidal disorders and listing clinical features. It also covers etiology, pathogenesis, diagnosis and treatment of Parkinson's disease.
EEG in idiopathic generalised epilepsiesNeurologyKota
This document provides information on idiopathic generalized epilepsies (IGE), which are a group of epilepsy disorders characterized by generalized bilateral spike-wave complexes on EEG. It describes the main seizure types seen in IGE including absence seizures, myoclonic seizures, and generalized tonic-clonic seizures. It also discusses several specific IGE syndromes like childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy. For each syndrome it provides details on clinical presentation, EEG features, treatment approaches, and prognosis.
Mid brain anatomy and vascular syndromesNeurologyKota
The document discusses midbrain syndromes caused by lesions in different areas of the midbrain. It describes the anatomy and vascular supply of the midbrain. It then explains several midbrain syndromes - Parinaud's syndrome causes limited upward gaze; Claude's syndrome results in ipsilateral oculomotor palsy and contralateral ataxia; Benedikt's syndrome includes oculomotor palsy, ataxia, and contralateral hemiparesis; Weber's syndrome involves CN III palsy, contralateral hemiparesis and lower facial weakness. Nothnagel's syndrome involves oculomotor palsy and ipsilateral ataxia. The midbrain contains the superior and inferior
The document discusses mesial temporal lobe epilepsy (MTLE), including its history, epidemiology, etiology, pathophysiology, clinical presentation, diagnosis, and treatment. MTLE is characterized by seizures originating in the mesial temporal lobe and is often associated with hippocampal sclerosis that can be identified on MRI. Diagnosis involves a combination of clinical presentation, EEG, functional imaging like PET and SPECT, and sometimes invasive monitoring to localize the seizure focus.
Temporal lobe epilepsy (TLE) is characterized by recurrent seizures originating from the temporal lobe. Hippocampal sclerosis, involving cell loss in the hippocampus, is the most common pathological finding in TLE. Auras occur in about 80% of temporal lobe seizures and can involve somatosensory, special sensory, autonic, or psychic symptoms. Diagnostic workup involves brain imaging like MRI and PET, as well as EEG to identify abnormalities in the temporal lobe.
Neurology 7th the atypical parkinsonian disordersRamiAboali
This document discusses various parkinsonian disorders including Parkinson's disease, atypical parkinsonian disorders (Progressive supranuclear palsy, Multisystem atrophy, Corticobasal degeneration), and other causes of parkinsonism such as medications, cerebrovascular disease, Wilson's disease, and Huntington's disease. It provides details on the clinical features, investigations, pathology, and management of these conditions.
Mesial temporal lobe epilepsy involves seizures originating in the mesial temporal lobe structures like the hippocampus and amygdala. Key features of mesial temporal lobe epilepsy include focal seizures with impaired awareness that involve automatisms and psychic symptoms. Diagnosis involves EEGs that may show interictal temporal sharp waves, spikes or slow waves as well as postictal changes that can lateralize the seizure onset. Resection of the epileptogenic mesial temporal lobe structures is an effective treatment for drug-resistant mesial temporal lobe epilepsy.
Continuous spike and wave during slow wave sleep(CSWS)Faizan Abdullah
continuous spike and wave during slow wave sleep(CSWS) was first described by patry.
The syndrome is characterized by continuous spike and wave activity during non-REM sleep and is sometimes called as “Epilepsy with electrical status Epilepticus during slow sleep” (ESES ).
Onset ranges from 1-12 years peak age around 8 years.
2/3 of patients normal neurologically before onset. In time most patients have frequent seizures generalized tonic clonic , atypical absence and atonic also have a significant decline in IQ with deterioration in language, impaired memory , reduced attention span, and behavioral changes with aggression or psychosis epileptiform activity consists of generalized slow 1.5 to 2.5HZ spike wave as well as focal or multifocal spikes, which are sporadic in the waking state.
In sleep, spike-wave bursts become nearly continuous(CSWS pattern) , occupying more than 85% of the total NON-REM sleep time .
The csws pattern persists for one to several years. Similar to LKS, the EEG then tends to normalize and seizures remit spontaneously in most patients.
However recovery of neurological deficit and behavior is often incomplete and about half of the patients remain profoundly impaired.
Nervous system normal and abnormal findingsMelz Susan
This document provides guidance on assessing the nervous system in geriatric patients. It lists normal findings such as reduced nerve cells and cerebral blood flow. It also lists abnormal findings including increased risk of falls, short term memory loss, Alzheimer's disease, Parkinson's disease, epilepsy, dementia, stroke, and depression. The document instructs nurses to illustrate and paste examples of five normal and abnormal findings for the nervous system on an illustration board as part of a classroom activity.
This patient presented with right third nerve palsy, lateral rectus paralysis, and pain and numbness in the distribution of the first and second divisions of the fifth nerve. This clinical presentation suggests a lesion in the superior orbital fissure, which contains the third, fourth, and first and second divisions of the fifth cranial nerves as they exit the skull. Lesions in this area can be caused by conditions like Tolosa-Hunt syndrome, pituitary tumors, nasopharyngeal metastases, cavernous aneurysms, or herpes zoster infection.
This document summarizes key aspects of coma and brain stem death. It discusses the neurological structures involved in consciousness and what is required to induce coma. Coma is defined as unarousable unresponsiveness, distinguished from an alert state. Assessing a comatose patient involves obtaining history, performing a general and neurological exam including the Glasgow Coma Scale, and considering appropriate investigations and management. Brain death is defined as the irreversible loss of all brain functions including the brainstem, determined by coma, absence of brainstem reflexes, and apnea on testing.
Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by parkinsonism, cerebellar ataxia, and autonomic failure. It was previously known as several other names. MSA has two phenotypes - parkinsonian (MSA-P) and cerebellar (MSA-C) - defined by their predominant motor abnormalities. Autonomic failure is widespread in MSA and affects control of functions like blood pressure and bladder control. MSA is characterized neuropathologically by protein inclusions in oligodendrocytes and the absence of Lewy bodies.
This document discusses the motor nervous system and motor paralysis from multiple levels including:
- The motor cortex and its connections to other brain areas
- The extrapyramidal and pyramidal systems
- Different types of apraxia and their lesion locations
- Lesions of the brainstem, spinal cord, nerves and muscles that can cause hemiplegia, monoplegia, or paraplegia
- The clinical features and localization of upper and lower motor neuron lesions
- Specific motor syndromes and their etiologies
It provides an overview of the organization of the motor system and localization of lesions throughout the nervous system that can result in different clinical motor deficits.
There are extensive number of neurodegenerative diseases but i have briefly discuss about the eight disease conditions. Hopefully it will be helpful to prospect learner. Good Luck
Coma and brain death are discussed. Coma is defined as an unresponsive state where only brainstem reflexes remain. Causes of coma include metabolic disturbances, structural lesions, and brainstem lesions. Examination of comatose patients involves assessing motor responses, breathing patterns, pupil size/reactivity, and reflexive eye movements. Brain death is the irreversible loss of brain and brainstem function, inevitably leading to organ failure. Diagnosing brain death requires determining the cause is sufficiently severe, no improvement after treating reversible causes, and absence of brainstem reflexes over an observation period.
Pierre Flourens promoted the idea that the cerebral cortex is not functionally subdivided. He used experimentation on dogs and pigeons, removing parts of their brains and noting behavioral changes, finding loss of coordination when removing the cerebellum. Paul Broca was the first to find localization of function in the cerebral cortex by examining a patient with speech inability and discovering the involvement of the left frontal lobe. Studying the nervous system and brain localization of function has been important to understanding psychology and behavior.
Hereditary spastic paraplegia (HSP) is a group of inherited neurological disorders characterized by progressive spasticity and weakness in the lower limbs. HSP can be caused by mutations in several genes and is inherited in autosomal dominant, recessive, mitochondrial or X-linked patterns. Symptoms usually begin between ages 20-40 and include difficulty walking, dragging toes, increased muscle tone and reflexes in the legs. HSP is classified based on symptoms, age of onset, and inheritance pattern. While there is no cure, treatment focuses on physical therapy and medications to reduce spasticity.
Temporal lobe epilepsy is one of the most common forms of epilepsy. It can be caused by hippocampal sclerosis or lesions in the temporal lobe. Hippocampal sclerosis involves neuronal loss and gliosis in the hippocampus and is the most common pathological finding in temporal lobe epilepsy patients. Interictal EEG findings like temporal intermittent rhythmic delta activity and temporal sharp waves help lateralize the seizure focus. Video EEG monitoring helps capture seizures and interictal discharges. Treatment involves antiepileptic drugs and potentially resective surgery for drug-resistant cases.
Partial complex epilepsy is characterized by focal seizures that impair consciousness. It is most commonly caused by temporal lobe epilepsy but can arise from other brain regions. Diagnosis involves obtaining a detailed history, physical exam, EEG, and MRI brain imaging. Treatment includes antiepileptic medications and potentially surgery for drug-resistant cases. Surgical options include temporal lobectomy for temporal lobe epilepsy, which can cure seizures in over 50% of carefully selected patients. Prognosis depends on seizure frequency and underlying etiology.
Extrapyramidal System and Disorders of Extrapyramidal SystemChetan Ganteppanavar
The document discusses the extrapyramidal system and disorders of the extrapyramidal system. It begins by defining the extrapyramidal system as referring to the basal ganglia and array of brainstem nuclei. It then lists the components and tracts of the extrapyramidal system. The document goes on to discuss disorders like Parkinson's disease, classifying extrapyramidal disorders and listing clinical features. It also covers etiology, pathogenesis, diagnosis and treatment of Parkinson's disease.
EEG in idiopathic generalised epilepsiesNeurologyKota
This document provides information on idiopathic generalized epilepsies (IGE), which are a group of epilepsy disorders characterized by generalized bilateral spike-wave complexes on EEG. It describes the main seizure types seen in IGE including absence seizures, myoclonic seizures, and generalized tonic-clonic seizures. It also discusses several specific IGE syndromes like childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy. For each syndrome it provides details on clinical presentation, EEG features, treatment approaches, and prognosis.
Mid brain anatomy and vascular syndromesNeurologyKota
The document discusses midbrain syndromes caused by lesions in different areas of the midbrain. It describes the anatomy and vascular supply of the midbrain. It then explains several midbrain syndromes - Parinaud's syndrome causes limited upward gaze; Claude's syndrome results in ipsilateral oculomotor palsy and contralateral ataxia; Benedikt's syndrome includes oculomotor palsy, ataxia, and contralateral hemiparesis; Weber's syndrome involves CN III palsy, contralateral hemiparesis and lower facial weakness. Nothnagel's syndrome involves oculomotor palsy and ipsilateral ataxia. The midbrain contains the superior and inferior
The document discusses mesial temporal lobe epilepsy (MTLE), including its history, epidemiology, etiology, pathophysiology, clinical presentation, diagnosis, and treatment. MTLE is characterized by seizures originating in the mesial temporal lobe and is often associated with hippocampal sclerosis that can be identified on MRI. Diagnosis involves a combination of clinical presentation, EEG, functional imaging like PET and SPECT, and sometimes invasive monitoring to localize the seizure focus.
Temporal lobe epilepsy (TLE) is characterized by recurrent seizures originating from the temporal lobe. Hippocampal sclerosis, involving cell loss in the hippocampus, is the most common pathological finding in TLE. Auras occur in about 80% of temporal lobe seizures and can involve somatosensory, special sensory, autonic, or psychic symptoms. Diagnostic workup involves brain imaging like MRI and PET, as well as EEG to identify abnormalities in the temporal lobe.
Neurology 7th the atypical parkinsonian disordersRamiAboali
This document discusses various parkinsonian disorders including Parkinson's disease, atypical parkinsonian disorders (Progressive supranuclear palsy, Multisystem atrophy, Corticobasal degeneration), and other causes of parkinsonism such as medications, cerebrovascular disease, Wilson's disease, and Huntington's disease. It provides details on the clinical features, investigations, pathology, and management of these conditions.
Mesial temporal lobe epilepsy involves seizures originating in the mesial temporal lobe structures like the hippocampus and amygdala. Key features of mesial temporal lobe epilepsy include focal seizures with impaired awareness that involve automatisms and psychic symptoms. Diagnosis involves EEGs that may show interictal temporal sharp waves, spikes or slow waves as well as postictal changes that can lateralize the seizure onset. Resection of the epileptogenic mesial temporal lobe structures is an effective treatment for drug-resistant mesial temporal lobe epilepsy.
Continuous spike and wave during slow wave sleep(CSWS)Faizan Abdullah
continuous spike and wave during slow wave sleep(CSWS) was first described by patry.
The syndrome is characterized by continuous spike and wave activity during non-REM sleep and is sometimes called as “Epilepsy with electrical status Epilepticus during slow sleep” (ESES ).
Onset ranges from 1-12 years peak age around 8 years.
2/3 of patients normal neurologically before onset. In time most patients have frequent seizures generalized tonic clonic , atypical absence and atonic also have a significant decline in IQ with deterioration in language, impaired memory , reduced attention span, and behavioral changes with aggression or psychosis epileptiform activity consists of generalized slow 1.5 to 2.5HZ spike wave as well as focal or multifocal spikes, which are sporadic in the waking state.
In sleep, spike-wave bursts become nearly continuous(CSWS pattern) , occupying more than 85% of the total NON-REM sleep time .
The csws pattern persists for one to several years. Similar to LKS, the EEG then tends to normalize and seizures remit spontaneously in most patients.
However recovery of neurological deficit and behavior is often incomplete and about half of the patients remain profoundly impaired.
Nervous system normal and abnormal findingsMelz Susan
This document provides guidance on assessing the nervous system in geriatric patients. It lists normal findings such as reduced nerve cells and cerebral blood flow. It also lists abnormal findings including increased risk of falls, short term memory loss, Alzheimer's disease, Parkinson's disease, epilepsy, dementia, stroke, and depression. The document instructs nurses to illustrate and paste examples of five normal and abnormal findings for the nervous system on an illustration board as part of a classroom activity.
This patient presented with right third nerve palsy, lateral rectus paralysis, and pain and numbness in the distribution of the first and second divisions of the fifth nerve. This clinical presentation suggests a lesion in the superior orbital fissure, which contains the third, fourth, and first and second divisions of the fifth cranial nerves as they exit the skull. Lesions in this area can be caused by conditions like Tolosa-Hunt syndrome, pituitary tumors, nasopharyngeal metastases, cavernous aneurysms, or herpes zoster infection.
This document summarizes key aspects of coma and brain stem death. It discusses the neurological structures involved in consciousness and what is required to induce coma. Coma is defined as unarousable unresponsiveness, distinguished from an alert state. Assessing a comatose patient involves obtaining history, performing a general and neurological exam including the Glasgow Coma Scale, and considering appropriate investigations and management. Brain death is defined as the irreversible loss of all brain functions including the brainstem, determined by coma, absence of brainstem reflexes, and apnea on testing.
Multiple system atrophy (MSA) is a neurodegenerative disorder characterized by parkinsonism, cerebellar ataxia, and autonomic failure. It was previously known as several other names. MSA has two phenotypes - parkinsonian (MSA-P) and cerebellar (MSA-C) - defined by their predominant motor abnormalities. Autonomic failure is widespread in MSA and affects control of functions like blood pressure and bladder control. MSA is characterized neuropathologically by protein inclusions in oligodendrocytes and the absence of Lewy bodies.
This document discusses the motor nervous system and motor paralysis from multiple levels including:
- The motor cortex and its connections to other brain areas
- The extrapyramidal and pyramidal systems
- Different types of apraxia and their lesion locations
- Lesions of the brainstem, spinal cord, nerves and muscles that can cause hemiplegia, monoplegia, or paraplegia
- The clinical features and localization of upper and lower motor neuron lesions
- Specific motor syndromes and their etiologies
It provides an overview of the organization of the motor system and localization of lesions throughout the nervous system that can result in different clinical motor deficits.
There are extensive number of neurodegenerative diseases but i have briefly discuss about the eight disease conditions. Hopefully it will be helpful to prospect learner. Good Luck
Coma and brain death are discussed. Coma is defined as an unresponsive state where only brainstem reflexes remain. Causes of coma include metabolic disturbances, structural lesions, and brainstem lesions. Examination of comatose patients involves assessing motor responses, breathing patterns, pupil size/reactivity, and reflexive eye movements. Brain death is the irreversible loss of brain and brainstem function, inevitably leading to organ failure. Diagnosing brain death requires determining the cause is sufficiently severe, no improvement after treating reversible causes, and absence of brainstem reflexes over an observation period.
Pierre Flourens promoted the idea that the cerebral cortex is not functionally subdivided. He used experimentation on dogs and pigeons, removing parts of their brains and noting behavioral changes, finding loss of coordination when removing the cerebellum. Paul Broca was the first to find localization of function in the cerebral cortex by examining a patient with speech inability and discovering the involvement of the left frontal lobe. Studying the nervous system and brain localization of function has been important to understanding psychology and behavior.
Hereditary spastic paraplegia (HSP) is a group of inherited neurological disorders characterized by progressive spasticity and weakness in the lower limbs. HSP can be caused by mutations in several genes and is inherited in autosomal dominant, recessive, mitochondrial or X-linked patterns. Symptoms usually begin between ages 20-40 and include difficulty walking, dragging toes, increased muscle tone and reflexes in the legs. HSP is classified based on symptoms, age of onset, and inheritance pattern. While there is no cure, treatment focuses on physical therapy and medications to reduce spasticity.
Extrapyramidal system.pdf very good detailssudaisahmad16
The extrapyramidal system is a neural network located in the brain that is part of the motor system and centers around the indirect control of movement. It responds to purposive, nonvoluntary movements and regulates muscle tone. The basal ganglia are nuclei that are part of complex regulatory circuits connected to the motor cortex and exert excitatory and inhibitory effects on movement and muscle tone. Lesions can cause excess or deficiency of movement. Parkinson's disease is the most common basal ganglia disease.
Hereditary spastic paraplegia (HSP) is a group of inherited neurological disorders characterized by the progressive stiffening and weakening of the lower limbs. The most common symptoms are difficulty walking and lifting the toes. HSP results from degeneration of nerve fibers in the spinal cord that control the lower body, and can be caused by mutations affecting axonal transport, mitochondria, or myelin. While there is no cure, treatment focuses on physical therapy, medication to reduce spasticity and pain, and addressing complications like contractures.
This document discusses several topics related to brain function and neuroscience. It begins by describing arousal and attention, noting that arousal requires the ascending reticular activating system (ARAS) within the brainstem and projections to the thalamus. It then discusses emotion, noting that basic drives are centered in the limbic system while distinctly human emotions are represented in the cortex. Finally, it provides information on frontal lobe function, language, memory, and the limbic system.
The document summarizes several biological and sociological theories of schizophrenia. The biological theories discussed are the neurodevelopmental theory and the dopamine theory. The neurodevelopmental theory proposes that schizophrenia results from aberrations in early brain development. The dopamine theory attributes schizophrenia symptoms to disturbed dopamine signaling in the brain. The sociological theories discussed are stress theory, structural strain theory, and labeling theory. These theories suggest social and environmental factors can influence mental illness rates.
The nervous system, parts, function, illness and diseasesMariel Flores
The nervous system is the body's information gatherer, storage center and control system. It collects information from inside and outside the body and sends it to the brain for analysis, then sends signals to initiate responses. The nervous system consists of the central nervous system (brain and spinal cord) and peripheral nervous system (nerves connecting to the rest of the body). The peripheral system includes the somatic system for voluntary movement and autonomic system for involuntary functions like heart rate. The autonomic system has the parasympathetic and sympathetic divisions that work in opposition to regulate normal and stress responses. Common nervous system diseases include Alzheimer's, which causes dementia, and Parkinson's, characterized by movement issues from dopamine neuron loss.
neurobiology of brain and everyday behavioursakshipalod04
This is the final project for the course neurobiology of brain and behaviour. This consists analysis of the neurodegenerative disease- Amyotrophic lateral sclerosis (ASL)
The basal ganglia are subcortical brain structures involved in motor control and include the corpus striatum, amygdaloid body, and claustrum. The corpus striatum contains the caudate nucleus and lentiform nucleus, which regulate muscle tone and movement. Damage to the basal ganglia can cause movement disorders like Parkinson's disease due to reduced dopamine in the corpus striatum.
The document provides information on the anatomy and physiology of the nervous system. It discusses the three main parts of the nervous system: central nervous system (brain and spinal cord), peripheral nervous system (cranial and spinal nerves), and autonomic nervous system (sympathetic and parasympathetic). It describes the structures and lobes of the brain. It also outlines the general functions of the nervous system in controlling the body, receiving stimuli, and determining responses. The document then discusses assessment and examination of the nervous system, including consciousness, cranial nerves, motor skills, sensation, and reflexes. Finally, it covers various diagnostic tests and evaluations like CT scans, MRI, EEGs, and lumbar punctures to analyze CSF.
Neuropsychiatric Manifestation In 8 Years Old Girl Presented With Obstructive...AR Muhamad Na'im
This document summarizes a case report of an 8-year-old girl presenting with obstructive hydrocephalus secondary to a posterior fossa tumor. She exhibited neurological symptoms like lower limb weakness and worsening headaches, as well as psychiatric symptoms including hallucinations and delusions. Imaging showed a tumor in the posterior fossa and ventriculomegaly. Posterior fossa tumors can cause hydrocephalus by disrupting cerebrospinal fluid flow. While psychiatric issues are common post-resection, they can also arise from brain changes caused by the tumor. The patient's symptoms were likely due to the mass effect of the tumor and associated hydrocephalus.
The document discusses the history of schizophrenia from ancient times to modern day. It describes how schizophrenia was first identified as a distinct mental illness in 1887 by Emil Kraepelin. The term "schizophrenia" was coined in 1911 by Eugen Bleuler to describe symptoms of fragmented thinking and perception. It also provides statistics on the prevalence of schizophrenia and discusses potential causes like genetics, brain abnormalities, and environmental factors.
During my 1st &2nd year of residency period , i used to teach Anatomy and Orthopaedics for foreign undergraduate medical students. At last year i taught Neurology for one batch. so i posted some of my collections for competely educational purpose coz i believe in knowledge ...inseted of deleting these ppts , they may me useful for others so i shared it ....
This document discusses current trends in the management of spasticity in hemiplegic patients. It defines spasticity as a velocity-dependent increase in muscle tone caused by damage to the central nervous system. Spasticity can range from mild muscle stiffness to severe, painful muscle spasms. If left untreated, spasticity may lead to muscle contractures, deformities, and other complications. Common treatments discussed include oral medications, botulinum toxin injections, physical therapy, and the modified Ashworth scale for assessing spasticity severity.
The neurological examination aims to determine nervous system function, localize lesions, and arrive at diagnoses and prognoses. It involves obtaining a thorough history and performing hands-off and hands-on examinations. The hands-off exam observes mental status, posture, gait, and behavior without disturbing the patient. The hands-on exam evaluates the 12 cranial nerves and identifies abnormalities to localize lesions. Key tests include menace response, pupillary light reflexes, cranial nerve function, and neurological reflexes. Abnormal findings provide clues to diagnose conditions affecting the brain, spinal cord, or peripheral nerves.
The document discusses the evolution of nervous systems in invertebrates and vertebrates. It describes how invertebrates like sponges, cnidarians, flatworms, and mollusks have a ganglionic nervous system with nerve cords and ganglia. Vertebrates evolved a cerebrospinal nervous system with a centralized brain and spinal cord. The cerebrospinal system allows for more complex processing and specialized functions in different brain regions. Comparing nervous system organization across species provides insights into neurodegenerative diseases and potential new treatment strategies.
The document discusses coma, including its definition, causes, clinical assessment, investigations, differential diagnosis and management. Coma is characterized by a total lack of arousal and awareness lasting at least 1 hour. It can be caused by structural brain injuries or metabolic derangements and represents a severe impairment of cerebral function. A systematic clinical approach is needed to identify treatable causes of coma such as head injuries, infections, drugs or toxic exposures.
The document compares the nervous systems of invertebrates and vertebrates. Invertebrates have simpler nerve net or ganglionic nervous systems, while vertebrates have more complex and centralized brain-spinal or cerebrospinal nervous systems. The evolution of nervous systems increased complexity from nerve nets to ganglia to brains correlated with increasing complexity of movement and behavior. More complex nervous systems in vertebrates provide advantages but also vulnerabilities like different parts being susceptible to neurodegenerative diseases.
The document discusses the nervous system and coordination in animals. It describes how the nervous system consists of the central nervous system (brain and spinal cord) and peripheral nervous system (nerves). Neurons transmit signals in the form of electrochemical waves via axons and synapses. Reflexes are automatic responses to stimuli that involve reflex arcs through sensory neurons, interneurons, and motor neurons. The size of nervous systems varies greatly across species from a few hundred cells in worms to over 100 billion cells in humans. Malfunctions can occur due to various genetic, physical, or age-related causes and are studied in neurology.
This document summarizes the anatomy and functions of the corpus callosum, the largest commissure connecting the two cerebral hemispheres. It describes agenesis of the corpus callosum, a condition where the corpus callosum fails to develop. Common characteristics of people with agenesis include vision, motor, speech and language delays, and difficulties with social skills. The condition is diagnosed using brain imaging and treated through medications, therapies, and education.
The use of Nauplii and metanauplii artemia in aquaculture (brine shrimp).pptxMAGOTI ERNEST
Although Artemia has been known to man for centuries, its use as a food for the culture of larval organisms apparently began only in the 1930s, when several investigators found that it made an excellent food for newly hatched fish larvae (Litvinenko et al., 2023). As aquaculture developed in the 1960s and ‘70s, the use of Artemia also became more widespread, due both to its convenience and to its nutritional value for larval organisms (Arenas-Pardo et al., 2024). The fact that Artemia dormant cysts can be stored for long periods in cans, and then used as an off-the-shelf food requiring only 24 h of incubation makes them the most convenient, least labor-intensive, live food available for aquaculture (Sorgeloos & Roubach, 2021). The nutritional value of Artemia, especially for marine organisms, is not constant, but varies both geographically and temporally. During the last decade, however, both the causes of Artemia nutritional variability and methods to improve poorquality Artemia have been identified (Loufi et al., 2024).
Brine shrimp (Artemia spp.) are used in marine aquaculture worldwide. Annually, more than 2,000 metric tons of dry cysts are used for cultivation of fish, crustacean, and shellfish larva. Brine shrimp are important to aquaculture because newly hatched brine shrimp nauplii (larvae) provide a food source for many fish fry (Mozanzadeh et al., 2021). Culture and harvesting of brine shrimp eggs represents another aspect of the aquaculture industry. Nauplii and metanauplii of Artemia, commonly known as brine shrimp, play a crucial role in aquaculture due to their nutritional value and suitability as live feed for many aquatic species, particularly in larval stages (Sorgeloos & Roubach, 2021).
Unlocking the mysteries of reproduction: Exploring fecundity and gonadosomati...AbdullaAlAsif1
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Exposé invité Journées Nationales du GDR GPL 2024
Deep Software Variability and Frictionless Reproducibility
Hereditary spastic paraplagia 813
1. University Of Education Faisalabad Campus
Submitted by:
Abd ur Rehman
Class:
M.Sc Zoology(EV)
Roll No:
mcf1900813
Semester:
3rd
Submitted to:
Dr.Mohsin Ahsan
Topic:
Hereditary spastic paraplegia
Genetic spastic paraplegia (GSP) might be a party of picked up sicknesses whose rule highlight
might be a reformist advance issue. The disease invigorates reformist (spasticity) and withdrawal
inside the lower appendages. HSP is furthermore intimated as inherent spastic paraparesis,
familial spastic paraplegia, French settlement burden, Strumpell disorder, or Strumpell-Lorrain
defilement.
The signs are the aftereffects of the brokenness of long axons inside the medulla spinalis. Axons
are long, finger-like projections of neurons that pass on basic signs all through the systema
nervosum. However, since they're touchy, they're reliably among the central hardships of certain
neurodegenerative problems, causing results like muscle deficiency or deadness of furthest
points. The influenced cells are the fundamental engine neurons; as needs are, the affliction is an
upper mooter neuron upper engine neuron: Upper engine neurons (UMNs) might be a term
presented by neurons.
William Gowers in 1886. they're found inside the cerebral mantle and brainstem and give data
direct down to begin interneurons and lower engine neurons, which consistently obviously signal
muscles to contract or slacken up. UMNs inside the cerebral mantle is the most wellspring of
intentional unforeseen development.
They are the more noteworthy pyramidal cells inside the cerebral mantle. there's such a goliath
pyramidal cell called Betz cells and are found scarcely under the outside of the cerebral mantle
inside layer V of the primary engine zone. The phone collections of Betz cell neurons are the
most basic inside the cerebrum, pushing toward basically 0.1 mm in the assessment.
The basic engine space, or focal gyrus, is one of the fundamental colossal districts inside the
projection. The focal gyrus is that the most back gyrus of the projection and it lies ahead of the
crevice of Rolando. The pyramidal cells of the focal gyrus besides are called upper engine
neurons. The strands of the upper engine neurons experience out of the focal gyrus finishing
inside the brainstem, where they will decussate (consolidate) inside the lower medulla to make
2. the sidelong pyramidal bundle on all sides of the medulla spinalis. The strands that don't
decussate will encounter the medulla and keep making the head corticospinal plots. The upper
efferent neuron drops inside the medulla spinalis to the degree of the attractive nervus spinalis
root. At now, the upper efferent neuron neurotransmitters with the lower efferent neuron, the
entirety of whose axons innervate a fiber of striated muscle.
These neurons accomplice the cerebrum to the satisfactory level inside the medulla spinalis, from
which point nerve flags still the muscles utilizing the lower engine neurons. The synapse
glutamate grants the nerve primary impulses from upper to chop down engine neurons, where it's
apparent by glutamatergic receptors.
HSP is obviously not exactly a spastic loss of development yet it truly may show up and act
much as an equal as spastic diplegia. The beginning of HSP is exceptional with the spastic loss
of development. Despite this, a couple of identical enemies of spasticity drugs used in spastic
loss of development are now and again wont to treat HSP signs. inside the systema nervosum,
HSP is accomplished by surrenders in the vehicle of proteins, fundamental proteins, cell dealing
with proteins, lipids, and different substances through the cell. Long nerve strands (axons) are
influenced because basic distances make nerve cells especially delicate to surrenders in these
alluded to instruments.
The infection was first portrayed in 1880 by the German tactile framework master Adolph
Str�mpell. it had been depicted considerably more thoroughly in 1888 by Maurice Lorrain, a
French subject matter expert. by their commitment to depicting the affliction, it's truly called
Str�mpell-Lorrain tainting in French-talking nations. The term normal spastic paraplegia was
created by Anita Harding in 1983.
Signs constantly
Results rely upon such an HSP acquired. the most piece of the pollution is reformist spasticity
inside the lower limits because of the pyramidal engine structure: The pyramidal group gives
purposeful control of solid new developments. It includes two undeniable pathways, the
corticobulbar package and subsequently the pyramidal part. The pyramidal plot passes on engine
signs from the essential engine area inside the mind, down the medulla spinalis, to the muscles of
the limit compartment and appendages. Thus, this pack is connected with the persistent headway
of the muscles of the body.
This is like way prompts extravagant reflexes, extensor plantar reflexes, muscle insufficiency,
and variable bladder unsettling impacts. Besides, among the center consequences of HSP
likewise are remembered peculiar development and bother for strolling, reduced vibratory sense
at the lower legs, and
paresthesia:
People with HSP can encounter excellent weariness identified with focal systema nervosum and
neuromuscular issues, which might be debilitating. Beginning appearances are normally issued
with balance, hitting the toe, or floundering. Indications of HSP may start at whatever stage for
the duration of regular daily existence, from the earliest starting point to more settled than 60
years.
In case signs start during the auxiliary school years or later, by then spastic advance unsettling
sway routinely drives over a couple of years. Sticks, walkers, and wheelchairs may, in the end,
be required, however, two or three people never need help contraptions. Weakness has been
portrayed as impelling sooner in grown-up beginning structures.
Significantly more unequivocally, patients with the autosomal ruling unadulterated kind of HSP
uncover the typical facial and extraocular progression. Notwithstanding the way that jaw stun
3. could in like way be enthusiastic in more arranged subjects, there's no discussion fomenting
effect or bother in gulping. Farthest point solid strain and strength are normal.
Inside beyond what many would consider possible, the strong strength is reached out at the
hamstrings, quadriceps, and lower legs. The insufficiency is generally obvious at the iliopsoas,
tibialis anticus, and less significantly, hamstring muscles. inside the puzzling kind of distress,
extra appearances are open. These join fringe neuropathy, amyotrophy, ataxia, scholastic
debilitation, ichthyosis, epilepsy, optic neuropathy, dementia, deafness, or talk issues, gulping or
loosening up.
Anita Harding mentioned the HSP in an unadulterated and refined structure. Unadulterated HSP
gives spasticity inside the lower appendages, identified with bladder issue upsetting effect in like
way as the nonappearance of vibration affectability. On the contrary hand, HSP is evaluated as
flighty when lower part spasticity is gotten along with any extra neurological outcome.
This game-plan is enthusiastic and patients with complex HSPs are every so often chose as
having cerebellar ataxia to have spasticity, check (with spasticity), or leukodystrophy. a segment
of the qualities recorded under is portrayed in surprising contaminations in contrast with HSP
heretofore. Thusly, some key qualities cover with other ailment parties. Signs of procured spastic
paraplegia
Period of the beginning:
As of now, HSP has been named beginning stage starting at the start or later beginning in
adulthood. The hour of onsets has two inspirations driving generally essential at age 2 and
around age 40. Disclosures suggest that previous beginning outcomes in a thorough sickness
length without loss of ambulation or the necessity for the use of a wheelchair. This was
comparatively portrayed already, that later-beginning structures develop sooner.
Causes:
HSP might be a social event of acquired issues. It keeps general legacy regulates and might be
acquired in an autosomal winning. X-related kept legacy is a strategy for legacy where an
adjustment in a quality on the X chromosome makes undeniably the be dependably passed on in
people (who are from an overall perspective homozygous for the quality change since they have
one X and one Y chromosome) and in females who are homozygous for the quality change, see
zygosity. Females with one duplicate of the changed quality are transporters.
X-related legacy understands that the quality causing the brand name or the issue is designed on
the X chromosome. Females have two X chromosomes while people have one X and one Y
chromosome. Transporter females who have just one duplicate of the change don't by and large
pass on the aggregate, notwithstanding the way that limits in X-chromosome inactivation (known
as slanted X-inactivation), can incite fluctuating levels of clinical clarification in transporter
females since express cells will introduce one X allele and some will pass on the other. The
current check of sequenced X-related qualities is 499, and the aggregate, including hazily
depicted properties, is 983.
Autosomal winning:
Autosomal winning is one of the explicit ways that a brand name or struggle is regularly gone
down through families. In an autosomal pervasive tainting, on the off chance that you get the
impossible to miss quality from only one parent, you'll get the infection. Routinely, one among
the oldsters can in like way have the infection.
Genotypes:
4. The properties are appropriated SPG (Spastic improvement quality). The quality territories are in
the methodology: genetic material - arm group number. These assignments are for human being
qualities metaphorically. The territories might impact different creatures. Despite the number of
qualities identified to be known with this situation ~40% of suitcases authentically can't have
their inspiration identified. The table beneath SPG? is utilized to show a quality that has been
associated with HSP yet has not yet gotten a spot HSP quality.
Pathophysiology:
The significant part of HSP is a span-secondary axonal collapse. These fit in the cross and
uncrossed corticospinal plots to the legs and fasciculus graceless. The spinocerebellar plot is
included less appreciably. Neuronal cell assortments of deteriorating axons are protected and
there is no proof of essential demyelination. Loss of primary horn cells of the spinal cord is seen
at times. Dorsal origin ganglion, back roots, and edging nerves are not uncomplicatedly
affected.HSP influence a few pathways in locomotive neurons. many qualities were familiar and
associated with HSP. It stays a test to accurately set apart the inner members in every one of the
unfair pathways, primarily because plentiful characters have a range of capacity and are
associated with supplementary than one pathway.
Axon pathfinding:
Pathfinding is noteworthy for axon maturity to the correct point (for example another daring cell
or a muscle). decisive for this implement is the L1CAM quality, a cell plane glycoprotein of the
immunoglobulin superfamily. Changes prompt a shortage of-work in L1CAM are as well found
in another X-associated disarray. These issues show corticospinal packet weak spot (a brand
draw attention to of HSP). L1CAM partake in a bunch of cooperation's, restrict other L1CAM
atoms just as extracellular cell link particles, integrands, and proteoglycans or intracellular
proteins in the vein of ankyrins.
The pathfinding malformation happens using the association of L1CAM with neuropilin-1.
Neuropilin-1 connects with Plain-A proteins to shape the Semaphorin-3A receptor multifaceted.
Semaphorin-a3A then delivers in the ventral spinal line to show corticospinal neurons from the
midline spinal string/medullary crossroads. On the off possibility that L1CAM doesn't work
precisely because of a change, the corticospinal neurons are not synchronized to the right
location and the flaw occurs.
Lipid assimilation:
Axons in the central and periphery tactile framework are covered with security, the myelin layer,
to accelerate action conceivable causing. Odd myelination in the CNS is recognized in particular
kinds of HSP HSP. Several characteristics were associated with myelin disfigurement, to be
explicit PLP1, GFC2, and FA2H.[3] The progressions change myelin union, thickness, and
uprightness.
The endoplasmic reticulum (ER) is the critical organelle for lipid blend. Changes in qualities
encoding proteins that have a limit in forming ER morphology and lipid ingestion were related to
HSP. Changes in ATL1, BSCL2, and ERLIN2 change ER structure, unequivocally the round and
empty affiliation and the improvement of three-way crossing focuses in ER tubules.
Many changed qualities are related to unusual lipid assimilation. The most generally perceived
impact is on arachidonic damaging (CYP2U1) and cholesterol (CYP7B1) retention,
phospholipase advancement (DDHD1 and DDHD2), ganglioside strategy (B4GALNT-1), and
the understanding among starch and fat preparing (SLV33A1).
Endosomal managing:
5. Neurons take in substances from there incorporating endocytosis. Endocytic vesicles break to
endosomes to convey their substance. Three rule compartments have endosomes managing:
Golgi to/from endosomes; plasma layer to/from early endosomes (through reusing endosomes)
and late endosomes to lysosomes. The brokenness of endosomal managing can have
extraordinary outcomes in motor neurons with long axons, as declared in HSP.
Changes in AP4B1 and KIAA0415 are associated with a disturbance in vesicle advancement and
layer managing including specific take-up of proteins into vesicles. The two characteristics
encode proteins that interface with a couple of various proteins and upset the secretory and
endocytic pathways.
Conclusions:
Starting assessment of HSPs depends on family parentage, the presence or nonattendance of
extra signs, and the prevention of other nongenetic purposes behind spasticity, the last being
especially tremendous in eccentric cases.
Cerebral and spinal MRI is a basic technique performed to obstruct other reformist neurological
conditions, for example, exceptional sclerosis, yet despite perceiving related irregularities, for
example, cerebellar or corpus callosum decay comparably as white issue assortments from the
norm. Differential assessment of HSP ought to additionally confine spastic diplegia which gives
essentially hazy standard impacts and even is treatable with comparative cures, for example,
baclofen and solid activity; sometimes, these two conditions may look and feel so equal that the
single saw separation might be HSP's gained nature versus the unequivocally non-characteristic
nature of spastic diplegia (in any case, as opposed to spastic diplegia and different sorts of
spastic cerebral loss of movement, HSP can't be continually treated with explicit dorsal
rhizotomy).
A definitive affirmation of HSP assessment should be given through completing acquired tests
focused on known inborn changes.
Treatment:
No particular treatment is realized that would forestall, slow, or switch HSP. Accessible
treatments primarily comprise of indicative clinical administration and advancing physical and
passionate prosperity. Therapeutics offered to HSP patients include: