October 1, 2021 Neuro with Sir Gebrielle Hipolito PDF

10-01-21 NEURO WITH SIR GEBRIELLE 2) TEMPORAL LOBE (Wernicke’s Speech HIPOLITO Area / PROBLEM IN COMPREHENSION ALZHEIMER’S DISEASE - WERNICKE’S APHASIA OR RECEPTIVE...

10-01-21 NEURO WITH SIR GEBRIELLE 2) TEMPORAL LOBE (Wernicke’s Speech HIPOLITO Area / PROBLEM IN COMPREHENSION ALZHEIMER’S DISEASE - WERNICKE’S APHASIA OR RECEPTIVE APHASIA – Difficulty in understanding – - most common form of dementia spoken and written language - Cause: IDIOPATHIC / Unknown - Confusion, limited ability to comprehend Risk Factors: instructions especially when spoken - Advancing Age (average onset at 50 y/o - by family history Both types can exist simultaneously, known as - common in women GLOBAL or MIXED Aphasia This progressive memory loss will eventually lead to Aphasia- A – ABSENCE – Inability to communicate loss of cognition, coordination and muscle properly and coherently control Such progression leads to problems in breathing, where the client dies due to secondary complications like pneumonia - Neurotransmitter that is involved: LOW LEVELS OF ACETYLCHOLINE Hallmark Manifestation: - GRADUAL onset of RECENT MEMORY LOSS (ANTEROGRADE AMNESIA) - early onset - BEHAVIORAL CHANGES : Wandering as the disease progresses to EVEN LATER Behavior / hallucination – late progression STAGES: A – Ataxia – Inability to perform coordinated general movements (walking, running and sitting) - Uncoordinated movements which are jerky, leading to increased risk for injury C – Cognitive Changes – Impaired thought process: hallucinations/illusions - Aggressive behavior - Apathy Signs and Symptoms - Wandering behavior - (ALL OF THEM START WITH LETTER A – Atrophy of Muscles A!!!) - Leads to secondary complications such as A – Anterograde Amnesia (recent memory loss) PNEUMONIA, INCONTINENCE A – Agnosia (inability to recognize familiar and Diagnosis common objects) - Alzheimer’s is only confirmed via AUTOPSY A – Apraxia – (Instruct patient to button shirt, or tie only – the fact that they show these signs is shoe laces) – inability to do meaningful and intended only a consideration and autopsy is for movements CONFIRMATION - Presence of NEUROFIBRILLARY A – Aphasia – it depends – DAMAGE IN THE TANGLES in the brain tissue - Increase levels of TAU PROTEINS in nerve 1) FRONTAL LOBE, where the Broca’s tissue samples Speech area/ MOTOR movement is located – BROCA’S APHASIA or EXPRESSIVE Diagnostic Tools like: APHASIA - CT Scan, MRI, PET, Blood tests only serve - Difficulty in speaking and writing to rule out other causes of neurologic - Confusion, slurring and stuttering deficits  1) Recent Viral Illness - Influenza - Mononucleosis - Severe Acute respiratory Syndrome SARS-Cov2 (COVID-19) 2) Bacterial Infection - AGE r/t Campylobacter jejuni Management: 3) Vaccine Components Medications: to slow the progression of the - Influenza disease - HiB 1) Anti-cholinesterase - DOC: Donepezil (Aricept), Galantamine, Rivastigmine – medications that slow down the breakdown of ACETYLCHOLINE 2) Reminiscence Therapy - To stimulate the patient mentally 3) FOCUS IS SAFETY – SAFETY Signs and Symptoms - Never re-organize the environment around Hallmark Signs the patient - Avoid the use of extension cords - Associated with temporary, bilateral - Avoid throw rags ascending paralysis (starts at the toes up to - Ensure a well-lighted environment (use red, the neck) orange or yellow lights for elderly client) - Progression of paresis (weakness) to paralysis – 4) Complete vaccinations when it comes to TEMPORARY LOSS OF FUNCTION SUCH AS: FLU and PNEUMONIA Movement Bladder and bowel elimination Bloatedness due to gas distention Respiratory Failure (kasi nga neck down ang paralysis, the lungs will be impaired and it will pass) - OVERALL, THE PROGRESSION IS SELF-LIMITING - COMPLETE RECOVERY IS EXPECTED GUILLAN-BARRE SYNDROME (GBS) AFTER A FEW WEEKS, AS LONG AS THE CLIENT SURVIVES THE - Transient or Temporary neurologic deficit PROGRESSION stemming from an autoimmune response which results to transient polyradiculoneuropathy Polyradiculoneuropathy – Inflammatory response and damage to the nerves or spine which results to damage to the myelin sheath or axons (nerve fibers) Cause: - like most, IDIOPATHIC GBS TYPES Mechanism why it happened: AUTOIMMUNE 1) ACUTE INFLAMMATORY RESPONSE – the body attacks the nerves or the DEMYELINATING POLYNEUROPATHY spine tissue (AIDP) Triggers: - Most common variety of GBS (Ascending Paralysis) 4) MILLER-FISHER SYNDROM (MFS) variant - Presence of MOTOR DEFICITS (paralysis, of GBS weakness and atrophy of the muscles) Triad: - Presence of sensory deficits , sensation Ataxia (Paresis – weakness , numbness, tingling Areflexia sensation, inability to perceive pain and Opthalmoplegia – paralysis of eye muscles temperature changes) - This variety is associated with a recent infection of ZIKA VIRUS - Damage to the myelin sheath and axons - More common in men (nerve fibers) - Most cases do not feature limb paralysis or paresis (weakness) 2) ACUTE MOTOR AXONAL NEUROPATHY (ASCENDING PADIN) (AMAN) - PARALYSIS BUT SENSATION IS RETAINED - Most common variety in EAST ASIA - Associated with recent Campylobacter jejuni infection (AGE) - Presence of motor deficit (paralysis, weakness and atrophy) Diagnosis - SENSORY FUNCTION IS RETAINED AND 1) CT Scan, MRI, and PET Scan INTACT 2) CSF Analysis - Verify the presence of an inflammatory - Little to no damage to the myelin sheath response - Damage is focused on axons or nerve fibers ELEVATED PROTEIN LEVELS: Normal level: >>>>> PROGRESSIVE LOSS OF NEUROMUSCULAR FUNTCION Risk Factors 1) Progressive Degeneration of substantia nigra 2) Advancing age (50 y/o) 3) Recent Viral Illness (Mononucleosis, meningitis) especially in elders- trigger autoimmunity 4) Knots or clumps of alpha-synuclein (LEWY BODIES) in the sustantia nigra – genetic in nature inherited or FAMILY HISTORY 5) Neuroleptics – cause FALSE Parkinson’s or 4) POSTURAL CHANGES Pseudoparkinsonism (lowers Dopamine - Considered as late onset levels) - Formations of generalized stiffness from 6) Substantia nigra deterioration is more head to toe common in Males - client tends to waddle, shuffle and develop a 7) Overexposure to toxins or pesticides hunched back during movement or at rest 8) No absolute causation, the disease is 5) LOSS OF AUTOMATIC MOVEMENTS IDIOPATHIC - Considered as late onset - Inability to perform movements such as blinking, frowning, grimace and follow-up of swing-through arms when ambulating. - this leads to hypomimia: ALSO KNOWN AS MASKED FACE – inability to express facial movements and expression Signs and Symptoms - The diagnosis of Parkinson’s disease is based on the presence and progression of the 5 CARDINAL SIGNS eventually the progression will influence basic functions such as breathing, eating and 1) UNINTENTIONAL TREMORS – first elimination. This decreases quality of life, observed manifestation (EARLIEST) leading to complications such as pneumonia which is a common complication that leads to - Resting tremors, stronger and more defined mortality. at rest. Moving the body part minimizes such tremors - Also known as “pill rolling” 2) RIGIDITY Management: - Slow onset of stiffness which can be unilateral or bilateral 1) Priority: SAFETY - can appear anywhere but most commonly - simple activities seen on upper limbs - mild to moderate exercise such as aerobic and weight bearing exercise 3) BRADYKINESIA - Rubberized grips for spoons other utensils - Slow movement with unsteady gait - Avoiding clutter in the home environment - Client compensates by dragging the feet - raised toilet seats and handlebars in the instead of lifting them; creating what is bathroom known as a shuffling gait 2) Diet : SOFT - Limited to pureed, mashed and ground food items 3) RESPIRATORY FUNCTION 4) ATROPHY PREVENTION Medical Management 1) a - Amantadine 2) b – bromocriptine 3) c – carbidopa 4) d – dopar or levodopa 4 – DOPAR/LEVODOPA = DOC – MOST EFFE