Cns final ppt

44
APPLIED ANATOMY OF CENTRAL NERVOUS SYSTEM Presented by- Prasad Bhadlikar Julies Sagare Abhishek ayarekar Vandana Dubey Sumit Mohite Khandu Chaudhari

description

 

Transcript of Cns final ppt

Page 1: Cns final ppt

APPLIED ANATOMY OF CENTRAL NERVOUS SYSTEM

Presented by-Prasad Bhadlikar Julies SagareAbhishek ayarekar Vandana DubeySumit Mohite Khandu Chaudhari

Page 2: Cns final ppt

WHAT IS A STROKE?

Brain tissue is damaged from a sudden loss of blood flow, resulting in a loss of neurological function

Causes: Blockage (blood clot) occurring inside a blood

vessel Blood vessel leaks blood due to rupture

Page 3: Cns final ppt

TYPES OF STROKES

Ischemic Stroke (85%)

Hemorrhagic Stroke (15%)

Page 4: Cns final ppt

Stroke affects people of

All Ages

All Ethnic Groups

All Backgrounds

Most strokes are preventable, take steps NOW to reduce having a stroke!

STROKE DOES NOT DISCRIMINATE

Page 5: Cns final ppt

SIGNS & SYMPTOMS OF STROKE

Sudden numbness or weakness of the face, arm, or leg, especially on one side of the body

Sudden confusion, trouble speaking or understanding

Sudden trouble seeing in one or both eyes

Sudden trouble walking, dizziness, loss of balance or coordination

Sudden, severe headache with no known cause

Page 6: Cns final ppt

RISK FACTORS FOR STROKE Family History of Stroke? Physical activity…less than a total of 30

minutes on most days? Man over age of 45, OR a woman over 55

years of age?

Risk factors you can control:

DIET - How we eat, do we follow our diet? EXERCISE - Do we exercise or get some physical

activity? MEDICATIONS - Taking medications correctly SMOKING - Stop smoking

Page 7: Cns final ppt

ONCE YOU ARE AT THE HOSPITAL

Diagnostic Testing

CT or MRI of the brain

EKG

Carotid Ultrasound

Echocardiogram

Page 8: Cns final ppt

EKG – may show atrial fibrillationCHEST X-RAY

Page 9: Cns final ppt

CAROTID ULTRASOUND – will show if there is stenosis (narrowing of the blood vessel)

Page 10: Cns final ppt

ECHOCARDIOGRAM – detects if any thrombus (blood clot) within the heart chambers

Any labs may be ordered, Lipid Profile (checking your cholesterol level) is done on all patients.

BLOOD WORK - LABS

Page 11: Cns final ppt

MEDICATIONS

Aspirin Aggrenox Plavix Blood pressure medication if

appropriate Cholesterol lowering

medicines if needed

Page 12: Cns final ppt

WHAT IS ALZHEIMER’S DISEASE

Alzheimer's disease (AD), also known as Senile Dementia of the Alzheimer Type (SDAT) or simply Alzheimer’s is the most common form of dementia. This incurable, degenerative, terminal disease was first described by a German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him.

Alzheimer's disease (AD) is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, and perception.

Many scientists believe that Alzheimer's disease results from an increase in the production or accumulation of a specific protein (beta-amyloid protein) in the brain that leads to nerve cell death.

Page 13: Cns final ppt

STAGES OF ALZZHEIMER’S DISEAASE

1)Earle Stage

2) Mild to Moderate Stage

3)Severe Stage

Page 14: Cns final ppt

DIAGNOSIS Alzheimer's disease is usually diagnosed clinically

from the patient history, collateral history from relatives, and clinical observations, based on the presence of characteristic neurological and neuropsychological features and the absence of alternative conditions.

Advanced medical imaging with computed tomography (CT) or magnetic resonance imaging (MRI), and with single photon emission computer tomography (SPECT) or positron emission tomography (PET) can be used to help exclude other cerebral pathology or subtypes of dementia.

The diagnosis can be confirmed with very high accuracy post-mortem when brain material is available and can be examined histologically.

Page 15: Cns final ppt

CAUSES OF ALZHEIMER’S DISEASES

Scientists don’t yet fully understand what causes AD, but it is clear that it develops because of a complex series of events that take place in the brain over a long period of time. It is likely that the causes include genetic, environmental, and lifestyle factors.

Some drug therapies propose that AD is caused by reduced synthesis of the neurotransmitter acetylcholine.

Other cholinergic effects have also been proposed, for example, initiation of large-scale aggregation of amyloid leading to generalized neuroinflammation.

Alzheimer's disease is characterized by a build-up of proteins in the brain. Though this cannot be measured in a living person, extensive autopsy studies have revealed this phenomenon. The build-up manifests in two ways:

Plaques– deposits of the protein beta-amyloid that accumulate in the spaces between nerve cells

Tangles – deposits of the protein tau that accumulate inside of nerve cells

Page 16: Cns final ppt

TREATMENT Although there is currently no way to cure

Alzheimer's disease or stop its progression, researchers are making encouraging advances in Alzheimer's treatment, including medications and non-drug approaches to improve symptom management.

Cholinesterase inhibitors increase the levels of acetylcholine in the brain, which plays a key role in memory and learning. This kind of drug postpones the worsening of symptoms for 6 to 12 months in about half of the people who take it. Cholinesterase inhibitors most commonly prescribed for mild to moderate Alzheimer's disease include Aricept (donezepil HCL), Exelon (rivastigmine), and Razadyne (galantamine).

Page 17: Cns final ppt

TREATMENT Aricept Used to delay or slow the symptoms

of ADDonepezil • Loses its effect over time • Used for mild, moderate and severe AD • Does not prevent or cure AD

CelexaCitalopram Used to reduce depression and anxiety • May take 4 to 6 weeks to work • Sometimes used to help people get to sleep

Depakote Used to treat severe aggressionSodium Valproate • Also used to treat depression and anxiety

Exelon Used to delay or slow the symptoms of AD Rivastigmine • Loses its effect over time • Used for mild to moderate AD • Can get in pill form or as a skin patch • Does not prevent or cure AD

Page 18: Cns final ppt

CONT...

Namenda Used to delay or slow the symptoms of ADMemantine • Loses its effect over time • Used for moderate to severe AD • Sometimes given with Aricept®, Exelon® • Does not prevent or cure AD

Razadyne Used to prevent or slow the symptoms of AD Galantamine • Loses its effect over time • Used for mild to moderate AD • Can get in pill form or as a skin patch • Does not prevent or cure AD

Zoloft Used to reduce depression and anxiety Sertraline • May take 4 to 6 weeks to work • Sometimes used to help people get to sleep

Trileptal Used to treat severe aggression Oxcarbazepine • Also used to treat depression and anxiety

Tegretol Used to treat severe aggression Carbamazepine • Also used to treat depression and anxiety

Remeron Used to reduce depression and anxiety Mirtazepine • May take 4 to 6 weeks to work • Sometimes used to help people get to sleep

Page 19: Cns final ppt

AMNESIA

A medical condition wherein a person may suffer from unusual forgetfulness which may cause memory loss is known as amnesia. It may result into:

Unable to learn or remember new events Unable to recall memories of the past At times involves both It may either come slowly or suddenly. It may

either be temporary or permanent. However, often the reason behind memory loss is loss of concentration due to depression, which may not be called amnesia. Hence, a proper diagnosis is required in case of amnesia.

Page 20: Cns final ppt

TYPES The common forms or types of amnesia are: Retrograde amnesia: Here, the patient will fail to

recollect the memories that occurred before the onset of amnesia

Anterograde amnesia: The patient suffering from this form of amnesia will be unable to remember memories that occurred after the onset of amnesia.

Lacunar amnesia: In this type of amnesia, the patient is unable to remember or recollect a particular event.

Emotional or hysterical amnesia: It is a temporary condition caused due to psychological trauma.

Korsakoff amnesia: Memory loss due to chronic alcoholism

Posthypnotic amnesia: It mainly causes after a hypnosis session, when a person is unable to remember the events happened during the session.

Transient global amnesia: It is a spontaneous memory lost which can last for few minutes or even hours.

Page 21: Cns final ppt

SINGS AND SYMPTOMS

The various signs and symptoms of amnesia are:

The person may suffer from neurological problems like uncoordinated movements seizures, tremors etc.

Confusion about events and disorientation of time and place are common signs.

False recollections, invented events or memories misplace in time too, are commonly seen among people who suffer from amnesia.

Page 22: Cns final ppt

CAUSES

The causes of amnesia are: Damage to those areas of the brain that are

vital for brain functioning or processing. Stroke Lack of sufficient amount of oxygen reaching

to the brain Lack of proper nutrition Tumours in the brain, especially in those

parts which control the memory Seizures Epilepsy, when not treated on time

Page 23: Cns final ppt

CONTINUED....

Intake of alcohol for a long time, which may cause deficiency of vitamin B1 – thiamine

Electro-convulsive therapy, which is used to treat mental illnesses too causes amnesia. Here, the electric current passed through the brain can damage the memories.

Severe trauma, damage to the brain or head injury can cause partial amnesia or partial memory loss.

Certain medications Depression, schizophrenia, bi-polar disorder

Page 24: Cns final ppt

DIAGNOSIS AND TREATMENT

Diagnosis:A comprehensive test is required to diagnose amnesia. First and foremost, your detailed medical history will be required by the doctor. Later, he may refer you to get physical and cognitive examination done. The tests may include checking reflexes, sensory functions, memory evaluation, MRI and CT scan.

Treatment:Amnesia is a condition that cannot be fully cured. However, if the patient has forgotten a lot of things, he/she can start learning from the beginning, especially if he is in the occupational sector. He/she can use devices that can help remember events easily for instance: records in the diaries, note-pads, mobiles or laptops. There are hardly any medications that can cure amnesia, and enhance your memory.

Page 25: Cns final ppt

ALCOHOL - SAFE DRINKINGAustralian Standards

2 standard drinks per day2 alcohol-free days per weekNo more than 4 standard drinks on a single occasion

Even less for older adults

(Ref: www.alcohol.gov.au 2010

Page 26: Cns final ppt

ALCOHOL RELATED BRAIN INJURY NEUROANATOMY

Alzheimer’s Australia (2008)

Page 27: Cns final ppt

ABI = ACQUIRED BRAIN INJURYAny injury to the brain that occurs after birth.

Traumatic Brain Injury (TBI):Contact sports, work, assault, road accidents

Stroke or Cerebral Haemorrhage: Disruption of the blood supply to the brain

Alcohol and Drug Abuse:ARBI/ARBD = Alcohol related brain injury/disease/disorder

Hypoxia:Disruption of the oxygen supply to the brain (> 3 minutes)

Brain Tumour & Infectious Disease:Brain tissue can be damaged through cancer, meningitis and

encephalitis.Degenerative Neurological Conditions:

Unlike other forms of ABI, these conditions do not stabilize or improve with time. e.g. Alzheimer's, Parkinson's and multiple sclerosis.

Page 28: Cns final ppt

ALCOHOL RELATED BRAIN INJURY (ARBI)SOMETIMES REFERRED TO AS ARBD – ALCOHOL RELATED BRAIN DAMAGE

Cerebellar atrophy – poor balance & gait

Peripheral neuropathy – poor mobility & dexterity

Hepatic encephalopathy – chronic liver disease toxins leading to progressive memory loss, disorientation, tremors & dementia.

Frontal lobe impairments – behavioural changes; eg. disinhibition, aggression, irritability or impulsivity, “Impulse Control Disorder” Wernicke’s encephalopathy - acute neurological disorder due to thiamine (Vitamin B1) deficiency

Korsakoff’s dementia – severely impaired mentation (Ref:

www.betterhealth.vic.gov.au)

Page 29: Cns final ppt

Overall: studies show that alcoholics have shrunken brains

Page 30: Cns final ppt

EXECUTIVE DYSFUNCTIONLong-term drinkers experience difficulties with: Attention and concentration Planning, organisation, problem solving Complex, abstract and flexible thinking Initiative Emotional and behavioural change Self awareness and insight

Page 31: Cns final ppt

MEMORY IMPAIRMENT IN ARBI Primarily caused by thiamine deficiency It can occur at any stage of ARBI Due to haemorrhage in midline structures

in the brain “Amnestic Syndrome” Can range from mild

(benign forgetting, short term memory) to profound (disorientation and confusion).

In response they frequently : Fall back to long-term learned behaviours and

responses Fill the memory gaps with poorly constructed, made

up scenarios Engage in cyclic conversations, thoughts and actions

Page 32: Cns final ppt

COMMON TYPES OF CHALLENGING BEHAVIOUR IN ARBI Perseveration (repetitive or cyclic behaviours) Verbal Aggression Physical Aggression Sexually Inappropriate Lack of motivation Withdrawal & Social Isolation Antisocial Suspicion & Paranoia Confusion & Confabulation High Risk Behaviours Ongoing Intoxication

Page 33: Cns final ppt

ASSESSMENT FOR ARBI

Where ABI is suspected, evaluation includes:History Physical examinationNeurological examinationNeuropsychological examinationNeuroimaging

Structural Functional

Best evaluation involves weighing all of the above

Page 34: Cns final ppt

UNDER DIAGNOSISAlcohol abuse and ARBI is grossly under-diagnosed among the older population. • Alcohol problems may not be identified as the

awareness of ARBI is low among frontline workers in health and social care.

• Older people rarely access specialist alcohol services.

• Inaccuracy or inappropriateness of generic assessment/evaluation tools

• Symptoms masked by dementia or other age-related conditions

• The social stigma attached to ARBI; eg. hidden by relatives

Mc Cabe, L (2005)

Page 35: Cns final ppt

Older Person

Living with an ARBI

PreventionNew Vs

Long -TermHomeless

Coordinated Service Delivery

Establish Specialised

CareServices

Research Prevention

Service Improvement

Cultural

Education&

Training

Policy Recognition,Support &

Funding

Page 36: Cns final ppt

SUMMARYExcessive & prolonged alcohol

consumption can lead to changes to structure and function of multiple body organs and systems leading to premature ageing.

Brain changes in ARBI lead to: Reduced behaviour control including drinking A range of cognitive problems, including memory and

executive skills Changes to physical

functions Personality changes Unstable mood

36

Page 37: Cns final ppt

EPILEPSY

• Epilepsy is a common and diverse set of chronic neurological disorders characterized by seizures.

•  It is a paroxysmal behavioral spell generally caused by an excessive disorderly discharge of cortical nerve cells of brain and can range from clinically undetectable (electrographic seizures) to convulsions

Page 38: Cns final ppt

SIGNS AND SYMPTOMS• long term risk of recurrent seizures• tongue may be bitten

CAUSES• Brain injury to the fetus during pregnency• Birth trauma – lack of oxygen• Head trauma – e,g. car accident• Brain tumor & stroke• Infection e.g. meningitis

Page 39: Cns final ppt

TREATMENT

surgery or medication.

If epilepsy seizures are due to a tumor, abnormal blood vessels, or bleeding in the brain, surgery to treat these disorders may make the seizures stop.

Medication to prevent seizures, called anticonvulsants, may reduce the number of future seizures.

Page 40: Cns final ppt

MEDICATION Currently there are 20 medications approved by the Food and Drug Administration for the use of treatment of epileptic seizures : carbamazepine (common US brand name Tegretol), clorazepate (Tranxene), clonazepam (Klonopin), ethosuximide (Zarontin), felbamate (Felbatol),fosphenytoin (Cerebyx), gabapentin (Neurontin), lacosamide (Vimpat), lamotrigine (Lamictal), levetiracetam (Keppra), oxcarbazepine (Trileptal),phenobarbital (Luminal), phenytoin (Dilantin), pregabalin (Lyrica), primidone (Mysoline), tiagabine (Gabitril), topiramate (Topamax), valproate ), valproic acid (Depakene), and zonisamide (Zonegran). Most of these appeared after 1990

Page 41: Cns final ppt

PARKINSON’S DISEASE

Parkinson’s diseases affects the way you move. It happens when there is a problem with certain nerve cells in brain

The Nerve cells make an important chemical called dopamine. Dopamine sends signals to the part of brain that controls movement. It lets muscles move smoothly and do what you want.

 The pathology of the disease is characterized by the accumulation of a protein called alpha-synuclein into inclusions called Lewy bodies in neurons, and from insufficient formation and activity of dopamine produced in certain neurons within parts of the midbrain

Page 42: Cns final ppt

SYMPTOMS OF DISEASE The main symptoms are Tremor, it means shaking or trembling. Tremor affects hands,

arms, or legs Stiff muscles Slow movement Problems with balance or walking diagnosis and treatment

Common symptoms are Changes in memory, concentration Visual hallucinations Depression Sleep disturbance Muffled speech

Page 43: Cns final ppt

PARKINSON’S DISEASE DIAGNOSIS The neurologic examination In that doctor takes a medical history and perform

physical examination the Doctor asks the patient and the family members or friends about symptom and observe the patient asking him or her to walk around the room, sit down Stand up, and so on.

Diagnostic tests The MRI and CAT scan of the brain produce remarkable

anatomic pictures. The MRI and CAT scan of the brain of people with

Parkinson’s disease appear Normal. Hence with the help of symptoms and neurological

findings they match finding with Parkinson’s disease this diagnosis called as clinical diagnosis.

Page 44: Cns final ppt

TREATMENT OF PARKINSON’SMedication

Carbidopa- levodopa (parcopa )

Dopamine agonists

MAO B inhibitors

Catechol O- methyltransferase (COMT) inhibitors

Amantadine

Surgical procedures

Deep brain stimulation