Module 12: Neuro Disorders Adult (b) Flashcards
Seizures
-Description
- Sudden, Transient alteration in brain electrical function caused by an abrupt, explosive and excessive discharge of cerebral neurons
Seizures
-Causes
- Hypoglycemia
- Water intoxication — Hyponatremia
- Alcohol intoxication
- Fever
- Stress
- Cerebral lesions
- Biochemical disorders
- Trauma
Seizure Classification
-Types of Seizures
- Generalized Seizures — Originate in both sides of the brain simultaneously — arises from deeper subcortical region of the brain
- Focal (partial Seizures — Originate from ONE area of the brain — Seizure activity is limited to one hemisphere
—Seizure can manifest as motor or non-motor - Status Epilepticus — Seizure phase lasts longer than 5 minutes — Prolonged or recurrent seizure before fully regaining consciousness
—Needs Emergency intervention
Seizures
-Phases of Clinical Manifestation
- Pre-Ictal — Prodrome present — Ex: Some symptom like confusion or anxiety that indicates imminent seizure — Focal Auras
- Ictal — Ictus phase is when you have TONIC-CLONIC activity and is the ACTUAL seizure
- TONIC PHASE - Occurs as result of exitation of the subcortical, THALMUS, and brainstem area
- CLONIC PHASE - Occurs when seizure d/c is interrupted resulting in alternating contraction and relaxation of muscles - Postictal — manifest in a long deep sleep, headache, confusion, memory loss or aphasia
Seizure Consequences
- 250% increase in ATP consumption during seizure
- 60% increase oxygen consumption
- 250% increase in cerebral blood flow
- Available glucose and oxygen are depleted
- Increase lactate in the brain leading to cellular exhaustion and destruction
Delirium
-Patho
- ACUTE confused states are transient states of confusion or awareness
- Typically acute w/ an abrupt onset but can be gradual or insidious in onset which can be caused by some type of toxin exposure.
- Causes
- Drug intoxication; alcohol or drug withdrawal; electrolyte imbalance; neuro dz or trauma; heart, liver or kidney failure; febrile illness; Post-anesthesia
Delirium
-Clinical Manifestation
- Difficulty Focusing
- Restlessness or irritability
- Highly distraught
- Incoherent
- Delirium usually resolves w/in a few days of onset **
Dementia
-Patho
- Dementia is the progressive failure of cerebral and cognitive functions not caused by an imported level of consciousness, like a TBI
- Results in nerve cell degeneration and brain atrophy
- Typically there is a slow reduction in cognitive function and its usually insidious
- There are some potentially reversible causes of dementia including
- Infections caused by meningitis, encephalitis, or neurosyphilis; Vit B deficiencies, ETOH, sedatives.
- Rule out the above causes when evaluating pt w/ dementia
Dementia
-Permanent Causes
- Alzheimer’s
- Lewy body dementia
- Vascular Dementia
CLinical Manifestation
-Loss of recent and remote memory **
Dementia
-Creutzfeldt-Jakob
- NON-Reversible Neurologic disorder w/ abnormalities of gait, speech, and dementia.
- Caused by PRIONS, which are infectious particles of nucleic acid
Alzheimer’s
-Info
- Alzheimer’s is thought to have a genetic component regardless of subtype
- Familial AD — Autosomal dominant gene mutation that affects amyloid processing and clearance
- Non-Hereditary AD — Sporadic and generally late onset
Alzheimer’s
-Patho
- Patho is altered beta amyloid processing and the development of neurotoxic fragments in plaques and tangles
- Results in loss of neurons causing BRAIN ATROPHY
- As deep groves for in cerebral cortex, there is a loss in synapses and acetylcholine — Resulting in memory loss
- LONG prodromal dz before manifestations of AD are obvious
Parkinson’s
-Info
Primary and secondary Causes
- Primary Causes — Mostly idiopathic; 10% has familial association
- Secondary Causes
- Repeated head trauma
- Huntington’s disease
- Fragile X syndrome
- Neurosyphilis
- Toxin exposure
- MS
- Huge variety of other neurodegenerativa diseases
- Drug induced causes are usually reversible
Parkinson’s Disease
-Patho
- Results from degeneration of the pigmented dopaminergic neurons that are found in the SUBSTANTIA NIGRA
- Loss of pigmented neurons in the substantia nigra which secrete dopamine, results in dopamine deficiency
- Lewy bodies and amyloid plaques have been found in the brain of Parkinson’s sufferers so there is clearly some type of patho similarity to Alzheimer’s
- There is also general loss of basal ganglia, which are a group of structures near the thalamus that coordinate movement
Parkinson’s
-Clinical Manifestations
- Can start on one side of the body and progress
- Tremor is often the first symptom
- Symptoms include
- Rigidity of movement
- Loss of facial expression
- Propulsive gait
- Absent arm swing
Amyotrophic Lateral Sclerosis
-Info
- Results in progressive muscle weakness — Motor neuron degenerative disorder of upper and lower motor neurons
- Causes progressive weakness, Respiratory failure and death
- Normal intellectual and cognitive function - 3-5 year life expectancy
Brain Trauma
-Risk factors
- 6 months to 2 years
- School-age children
- Adolescents and young adults 15-35 yrs
- Increase in people over 70 yrs
- Men are 1.5 x as likely to sustain TBI
- Falls are the #1 cause of brain injury
Brain Trauma
-Primary and Secondary
- Primary head trauma is result of direct focal hit to the skull causing injury
- Secondary brain injury is an indirect injury often a result of a CVA, ischemia, hemorrhage, oxidative stress or inflammation
Brain Trauma
-Classification of Severity
- Mild — Momentary LOC — No MRI findings — N/V, HAs, confusion/disorientation
- Moderate — LOC for 30 minutes or more — Retrograde amnesia for 24 hrs — may have skull fracture — memory and attention deficits
- Severe — HALLMARK of severe brain injury is LOC for 6 hrs or more. — associated with Brainstem signs
Types of Head Trauma
- Blunt — Focal injury and Diffuse injury to the axon
- Penetrating
- Focal — Localized to site of impact; scalp lac; skull fracture; contusions; hemorrhage
- Polar —Coup Counrecoup — Brain bounces off skull — Ex: Car accident
- Chronic Traumatic Encephalopathy CTE — Football players, military, trauma survivors
Epidural Hematoma
-Info
- Bleeding between dura and skull
- Always ARTERIAL BLEEDS — DANGEROUS
- Process is — period of unconscious followed be a period of lucidity then return to unconscious
- S/Sx’s
- Drowsiness, seizure, confusion, headache, vomiting
Subdural Hematoma
- Bleeding between dura mater and brain
- Can be acute and develops w/in hours of injury or subacute and develop over 48 hrs to 2 weeks
- About 50% associated with skull fractures
- Can occur with falls in older adults
- In acute and subacute, the tearing of bridging veins that extend from the dura to the brain surface is the major cause of hematoma**
- Clinical manifestations
- Unconscious
- Respiratory depression
- Focal motor dysfunction
- Pupillary dilation
Intracerebral Hematoma
- Bleeding that most often takes place in the frontal and temporal lobes
- Caused by penetrating force or a shearing force that injures small blood vessels — also caused by hemorrhagic strokes
- Clinical manifestations include
- Increased ICP
- Decreased LOC or coma
- Positive babinski reflexes
- Changes in breathing
- Temporal lobe Herniation
Spinal Cord Injury
-Info
- Can be result of shearing, compression or penetrating trauma
- Secondary spinal cord injury occurs after the initial trauma
- Combination of vascular, cellular, and biochemical events that result in edema, ischemia, excessive stimulation by neurotransmitters, inflammation, oxidative damage, and cell death
Spinal Cord Injury
-Transient Vs. Permanent Loss of function & Sensation
- Depends on level and extent of injury
- After an acute injury you might have sudden loss of voluntary movements, sensation and spinal/autonomic reflexes below injury
- Reflexes usually return in a few weeks
Spinal Cord Injury
-Spinal Shock
- Occurs IMMEDIATELY s/p injury d/t continuous loss of impulses to the brain below area of spine injury
- S/Sx’s:
- All motor and sensory functions below the area of injury may cease, temporarily
- Bladder function, thermal control and circulation are impacted
- May last days to weeks and when it passes, reflex activity may return
Spinal Cord Injury
-Neurogenic Shock
- Occurs w/ Cervical or thoracic injury
- Loss of sympathetic outflow that results in unopposed parasympathetic input mediated by vagus nerve
S/Sx’s include:
- Vasodilation
- Hypotension
- Hypothermia
- Bradycardia
Spinal Cord Injury
-Autonomic Hyperreflexia
- This may follow after spinal shock — Injury above T5-T6
- Reflex sympathetic discharge w/ uncompensated cardiac response
- The unopposed sympathetic response causes diffuse vasoconstriction
- Raises BP
- Diaphoresis, blurred vision, severe HA - Essentially there is vasoconstriction below level of injury and vasodilation above the level of injury
S/Sx’s
- Paroxysmal HTN
- Pounding headache
- Blurred vision
- Bradycardia
Spondylosis
- The pars auricular is of the vertebral arch has degeneration and over time can have micro fractures
Spondylolisthesis
- Spondylolisthesis occurs when there is a shift forward of vertebrae (stress Fx and sliding of vertebra)
Spinal Stenosis
- Spinal stenosis is a narrowing of the spinal canal and is something that should always be in your differential list when considering someone who has leg pain w/ movement
Disk Degeneration & Herniation
- DDD is common in people over 30 yrs — 1/2 of adults have some compression — normal part of aging
- As nucleus palposus loses water and buoyancy, disk spaces narrow
- Result can be shrinkage of the nucleus palposus, disk protrusion, tear of the annulus and Herniation of the disk contents outside the disk space
Radiculopathy
- Herniation or pressure on the spinal cord from the disk
- This can result in nerve pain or Radiculopathy
- Pain is exacerbated by coughing sneezing or raising the leg
Radiculopathy
-Complications
- Most emergency consequence of nerve compression is CAUDA EQUINA or SADDLE ANESTHESIA.
- Can result in neurogenic bladder, absent reflexes and numbness
Ischemic Stroke
- Ischemic Strokes — inadequate blood supply that results in inadequate cell oxygen and death of tissue
- Thrombotic Strokes — atrial occlusion by a thrombus that is formed in the brain or intracranial vessels
—Can be from Atherosclerosis or stenosis - Embolic stroke — fragments break from a thrombus formed outside the brain —Ex: A fib, fat or air emboli
Hemorrhagic Stroke
- Result of spontaneous bleeding in the brain — Less common
- Risk factor - Long-standing HTN; ruptured aneurysm
Intracranial Aneurysm
- Can result from:
- arteriosclerosis; congenital; trauma; vascular wall stress - Can cause remodeling, thickening and angiogenesis
Intracranial aneurysms
-Subtypes
- Saccular (berry) — small sacs that expand over time — caused by congenital malformation or vessel wall stress and inflammation
- Highest risk of rupturing between 20-50 yrs old - Fusiform — GIANT aneurysms in basilar artery or terminal carotid arteries — D/t arteriosclerotic changes
- Mycotic aneurysms — rare and the result of bacterial infection
- Traumatic dissecting aneurysms — weakening of arterial wall d/t trauma — might occur during embolization
Meningitis
- Inflammation of the brain or spinal cord
- Microbial invasion of the CNS
- It is more common to be caused by bacterial invasion — Can also be caused by viruses, fungi or parasites
Bacterial Meningitis — Pyogenic (pus forming) infection that invades the pia mater and arachnoid
Encephalitis
- Acute febrile illness that is an infection of the brain itself — Usually viral origin w/ nervous system involvement
- Most common forms caused by — Mosquito borne illness; HSV
- As viruses enter the CNS, edema and necrosis develop — Can progress to increased ICP and Herniation
S/Sx’s
- Altered mental status
- Delirium
- Unconsciousness
- Seizure
- Cranial nerve palsies
- abnormal reflexes
Multiple Sclerosis
- Progressive, inflammatory, demyelination, autoimmune disorder of the CNS — Results in scaring and loss of axons
- Myelin auto antigens trigger production of antibodies that cause demyelination
- S/Sx’s
- People may have optic neuritis or cerebelar syndromes that show gait instability, lack of coordination, tremor or ataxia - Causes are vitamin D deficiency — ages between 20-40 and females are 2x more likely to get MS
Guillain Barre
- Acquired inflammatory disease that causes demyelination of the PERIPHERAL NERVES w/ relative sparing of axons
- Acute onset w/ a characteristic ascending motor paralysis
- Demyelination is progressive from distal to próxima
- Caused by Zika, URI, GI infection, Flu vaccine
- Manifestation — Most significant consequence can lead to RESPIRATORY MUSCLE involvement w/ mechanical ventilation
- Recovery is slow but does occur
MS Vs Guillain Barre
- MS is a CNS disorder & Guillain Barre is PNS
2. MS causes scaring and loss of axons — Guillain Barre is axon sparing
Myasthenia Gravis
- Chronic inflammatory disorder where acetylcholine receptor antibodies attack the neuromuscular junction
- Main defect is T-cell dependent autoantibodies - Treatment for Myasthenia Gravis is REMOVAL of the THYMUS
- Clinical Manifestations
- Generalized weakness — starting at the head, face and neck
- Weakness and fatigue of the muscles of the eyes and throat — Diplopia & difficulty chewing, talking, swallowing - Treatment
- Anticholinesterase drugs, steroids, immunosuppressive, potential surgery
Schizophrenia
Term used to describe thought disorders
- Advanced imaging has found:
-Distinct, structural neuroanatomista altercation in this disorder including
—Enlargement of lateral and third ventricles
—Widening of the frontal cortical fissures and sul I
—Progressive loss of cortical gray matter in the frontal and temporal lobes - Causes
- Prenatal infection; perinatal complications; upbringing; Neurotransmitter hypothesis — alteration in brain dopamine pathways
Schizophrenia
-Hallmark S/Sxs
- Hallmark of schizophrenia is disorganized thought w/ positive and negative Sx’s
Mood disorders
- Mood refers to a sustained emotional state
- Biological factors that are theorized to contribute to depression
- Abnormal sleep
- Neurotransmission dysregulation — Reduced serotonin - Increased stress can cause chronic activation of the hypothalamic-pituitary adrenal system