Neurological Disorders Part 1 Flashcards

• CVD is a abnormality in brain caused by pathologic process in the blood vessels
• Two types of cerebrovascular disorders:
  • Ischemia with or without infarction
  • Hemorrhage
• Examples
  • Cerebrovascular accidents (CVAs) or strokes
  • Transient ischemic attacks (TIAs)
  • Aneurysms or malformations

pathologic process categories: lesions of the
vessel wall (e.g., aneurysm or malformations); occlusion of the vessel
lumen by thrombus or embolus; rupture of the vessel; and alteration
in blood quality, such as increased blood viscosity or clotting.

• Greatest risk factor: Hypertension

Types

• Ischemic: inadequate blood supply to brain from obstruction in arterial blood flow to the brain (thrombus, hypoperfusion of blood flow, embolus associated with atherosclerosis)
  • ischemia: inadequate cellular oxygen
• Hemorrhagic: Microaneurysms in these smaller vessels
• Because neurons surrounding the ischemic or infarcted areas
  undergo changes that disrupt plasma membranes, cellular edema
  results, causing further compression of capillaries.

• Transient ischemic attacks
  • Neurologic deficits are not permanent
  • episodes of neurologic dysfunction lasting no more than 1 hour and resulting from focal cerebral ischemia
• Thrombotic stroke
  • Arterial occlusions are caused by thrombi formed in the arteries that
    supply the brain or in intracranial vessels
  • Is attributed to atherosclerosis and inflammatory disease processes
• Embolic stroke
  • Fragments break from a thrombus that is formed outside of the brain usually in the heart, aorta, or common carotid artery.
  • A second stroke usually occurs

In ischemic infarcts, the affected area becomes pale and softens 6 to 12 hours after the occlusion (white infarct). Necrosis, swelling around the insult, and
mushy disintegration appear by 48 to 72 hours after infarction.

• S/S depends on the artery affected
  
  • Contralateral weakness in arms, legs, and/or face
  • Possible motor, speech, and/or swallowing problems

Contralateral sensory and motor manifestations occur on the opposite side of the body from the location of the brain lesion because motor tracts originate in the cortex and most cross over in the medulla.

• Thrombolysis (tissue-type plasminogen activator) is administered
  within 3 hours and up to 4 ½ hours of symptom onset for embolic
  stroke
• Not a treatment for a hemorrhagic stroke
• Hypertension is NOT aggressively treated

Acute ischemic stroke frequently presents with hypertension, but the systemic blood pressure should not be treated unless the systolic pressure is 150 to 220 mmHg or mean arterial pressure exceeds 150 mmHg. Overly aggressive treatment of hypertension can compromise collateral perfusion of the ischemic penumbra.

• Pharmacologic
  
  • Aspirin
  • Systemic anticoagulation
  • Thrombolysis
  • Antiplatelet therapy and statins to decrease recurrence
• Surgery
  
  • Endarterectomy- surgery to remove plaque

Treatment of ischemic stroke is focused on:
(1) restoring brain perfusion in a timeframe that does not contribute to
reperfusion injury (2) counteracting the ischemic cascade pathways
(3) lowering cerebral metabolic demand so that the susceptible brain
tissue is protected against impaired perfusion (4) preventing recurrent ischemic events (5) promoting tissue restoration

• Hemorrhagic stroke
  
  • Is spontaneous bleeding into the brain
• Clinical manifestations
  • Focal neurologic deficits, altered consciousness, headache
• Treatment
  
  • Needs to be initiated within 3–4 hours of symptom onset for reversibility of brain ischemia
  • Limit hematoma enlargement by managing HTN
  • Prevent or control seizures and cerebral edema Osmotic therapies (e.g., mannitol) are used for the treatment of IICP and cerebral edema in hemorrhagic stroke.

• Blood escapes from defective or injured vasculature into the subarachnoid space
• Blood produces an inflammatory response
• Greatest risk factor is family history
• Mortality rate is 50%

• Leaking vessels:
  • episodic headache
  • transient changes in mental status or level of consciousness
  • focal neurologic defects including visual or speech disturbances
  • stiff neck
  • nausea or vomiting
• Ruptured vessel causes: A ruptured vessel causes a sudden throbbing, “explosive” headache accompanied by nausea and vomiting, visual disturbances, motor deficits, and loss of consciousness related to a dramatic rise in ICP.
  • sudden throbbing “explosive” or “thunderclap” headache associated with nausea and vomiting
  • visual disturbances
  • motor deficits
  • loss of consciousness
• meningeal irritation and inflammation
• neck stiffness (nuchal rigidity)
• photophobia, blurred vision, irritability, restlessness, and low-grade fever
• Positive Kernig sign and Brudzinski sign

positive Kernig sign (straightening the knee with the hip and
knee in a flexed position produces pain in the back and neck regions)
and a positive Brudzinski sign (passive flexion of the neck produces
neck pain and increased rigidity)

• Treatment
  
  • Nimodipine (prevent vasospasm)
• Surgery: to clip the aneurysm

• Is a symptom of disease, not a specific disease

• Seizure:
  • is a sudden, transient disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons

• Epilepsy:
  • is a recurrence of seizures and a disorder for which no cause can be found
• Convulsion:
  • is tonic-clonic (jerky, contract-relax) movements associated with some seizures

Diseases and conditions associated with seizure disorders: Any condition that affects the CNS or neuronal environment

• Genetic predisposition
• Congenital malformations
• Perinatal injury
• Metabolic disorder
• Postnatal trauma
• Infection
• Brain tumor
• Vascular disease
• Drug/alcohol abuse

• Generalized seizures: affect neurons bilaterally
• Focal (partial) seizures: affect neurons unilaterally
• Epilepsy syndromes: genetic/developmental cause
• Unclassified epileptic seizures: etiology unknown
• Status epilepticus
• Is a medical emergency bc medical emergency because of the resulting cerebral hypoxia.
• Continuing/recurring seizures with incomplete recovery, unrelenting seizure activity that lasts 30 minutes or more

Clinical manifestations

• Depends on the type of seizure
• With clonic-tonic movements, the seizure may have an aura or a prodrome

Seizure sequence

• Resting potential instability
• Seizure initiation
• Bursts of action potentials
• Tonic phase
• muscle contraction with increased muscle tone
• Clonic phase
• alternating contraction and relaxation of muscles
• Postictal state: follows the seizure

Consequences

• Cerebral blood flow increases
• Cerebral oxygen consumption is increased by 60%.
• Glucose depletion
• Accumulation of lactate in brain tissues

• Antiseizure medication
• Ketogenic diet for epilepsy
• Surgery; vagal nerve stimulation

• Most common type of seizure in pediatric patients
• Usually develops within 24 hours of the onset of a fever (temp is usually >102)
• Usually develop between 6 months and 5 years of age
• Usually lasts less than 5 minutes
• Need to rule out meningitis by exam/testing
• Most children do not develop epilepsy after experiencing febrile seizures but a small percent can develop epilepsy

• Sensation of spinning (NOT lightheadedness)

occurs with inflammation of the semicircular canals or displacement of otoliths in the utricle and saccule of the semicircular canal system

• Peripheral Vertigo
• Benign paroxysmal positional vertigo (BPPV)
• Meniere disease
• Acute labyrinthitis and vestibular neuritis

• Central Vertigo

• Caused by strokes, tumors

• Medication-induced

• Anticonvulsants, salicylates, antibiotics

• Benign paroxysmal positional vertigo (BPPV)
• calcium deposits or debris in the posterior semicircular canal
• Treatment
  • Epley maneuvers- turning your head in a series of movements.

• Increased volume of endolymph in the semicircular canals
• Also have S/S vertigo + tinnitus and hearing loss
• Treatment
  • Benefit from a low sodium diet and should minimize use of alcohol and caffeine

• Most often caused by inflammation from a viral infection

• Caused by strokes, tumors

• Anticonvulsants, salicylates, antibiotics

• Bacterial meningitis
  
  • Infection of pia mater, arachnoid villi, subarachnoid space, ventricular system, and cerebrospinal fluid (CSF)
• Viral meningitis
  
  • virus enters the brain either directly or indirectly, through infected migrating leukocytes, and then infects vascular endothelial cells. The virus then enters the subarachnoid= meningitis
• Fungal meningitis
• Tubercular (TB) meningitis

• Bacterial

• Throbbing headache increasing in severity
• Increasing photophobia
• Nuchal rigidity
• Kernig sign
• Brudzinski sign
• Projectile vomiting

• Viral: Milder than bacterial meningitis

• Mild generalized throbbing headache
• Mild neck pain, stiffness
• Mild photophobia
• Fever, Malaise

• Most Common: Relapse-Remitting
  • S/S develop & resolve in a few weeks to months, returns to baseline → as times goes on relapse become more frequent(classic characteristic)
• Least Common: Primary-progressive
  • steady & gradual detetoriating w/o remission. gradual loss of power in the lower limbs that can be asymmetric, and bowel and bladder symptoms
• Secondary-progressive
  • replase-remitting, gradual worsening of the symptoms between relapses
• Progressive- relapsing
  • gradual deterioration, no remission, no return to baseline