ALTERATIONS IN NEUROLOGIC FUNCTION

1. ALTERATIONS IN NEUROLOGIC FUNCTION

2. Aging and the Nervous System • Decreasing Neurons • Memory Impairment • Decreasing Sensory and motor function • Decreasing Arterial blood flow • Neurotransmitter changes • Fibrosis of meninges • Medications

3. Coma: alterations in arousal • Structural locations • Supratentorial, infratentorial, subdural, extracerebral, intracerebral • Pathologic causes • Infectious, vascular, neoplastic, traumatic, congenital, degenerative, metabolic • All systemic diseases that cause CNS dysfunction are considered to be metabolic

4. Basic causes • Anything that increases intracranial pressure • Damage from hypoxia, hypoglycemia drugs, or toxins • Lesions or metabolic disorders that damage the RAS • Everything that goes to the cortex MUST pass through the thalamus via the RAS

5. Clinical Manifestations of Cerebral Dysfunction • Alterations in Levels of Consciousness indicate cortical dysfunction • Automatism • Confusion/Disorientation • Delirium/Lethargy • Stupor/Deep stupor • Coma • Light coma, coma, deep coma

6. Objective score—Glasgow Coma Scale • Used to give prognosis after head injury • Eye opening 1-4 • Best verbal response 1-5 • Best motor response 1-6 • Score > 11 85% have good recovery • Score 3--4 85% die or remain vegetative

7. Assess specific functions • Language and speech--L hemisphere • Dysarthria • Dysphonia • Aphasia

8. Breathing may be hemispheric or brain stem controlled • Hemispheric Patterns • Post hyperventilation apnea • Cheyne-Stokes respiration • Brain Stem Patterns • Central neurogenic hyperventilation • Apneusis • Cluster breathing • Ataxic breathing • Agonal gasps

9. Cranial nerves assess non-cortical function • I Olfactory • II Optic • III, IV, VI Control movement of eyes • V Motor & sensory to temporal and masseter muscles • VII Taste, muscles of facial expression • VIII Hearing and balance • IX, X Taste, swallowing, gag reflex • XI Flexors of neck, ability to shrug • XII Tongue muscles

10. Motor disruption may locate hemisphere and level • Purposeful (normal) • Inappropriate/not purposeful • Disruption of corticospinal system • Absent/unresponsive • Cortical shutdown • Thalamic disruption • Spinal cord lesions

11. Higher levels usually inhibit lower levels • Decorticate rigidity--arms flexed • damage above the midbrain • Decerebrate rigidity--exaggerated extension • damage to midbrain • Extensor in arms, flexion in legs • Pons dysfunctional • Flaccid--no response • Lower pons/upper medulla damaged

12. Upper motor neuron vs lower motor neuron • Muscle stretch reflexes (deep tendon reflexes) • LMN disease results in no reflexes of affected area only, flaccid paralysis, muscle atrophy • UMN disease initially areflexic, progressing to hyperreflexic, with spasticity as lose upper inhibition; minimal muscle atrophy

13. Seizure Disorders Relatively common (10% incidence) • Peak ages 1-10 years and > 60 years Look for underlying cause of xs neuronal discharge • head trauma with dura injury is predisposing factor Epilepsy is recurrent, spontaneous seizure pattern Primary epilepsy is usually idiopathic patient < 20 years old Secondary epilepsy has known trauma, infection, etc

14. Seizure Disorders--Classification Table 16-9 • Partial—conscious throughout • simple—lasts < 1 minute • complex—lasts 1-3 minutes • Generalized— involve entire cerebral cortex and diencephalon • lose consciousness, bilateral , symmetric • Specialized epileptic syndromes

15. Types of generalized seizures • Absence seizures (petit mal)—go vacant for a few seconds • Tonic-clonic seizures (grand mal) • incontinence, tongue biting, postictal phase with no memory of seizure • last 3-5 minutes, unconscious for another 30+ minutes • Increased HR, BP, body T, WBC count • fever convulsions—tonic-clonic seizures in children < 3 yrs

16. Status epilepticus • Continuous seizure activity of 20+ minutes • neurologic emergency with 22-25% mortality • IV diazepam; phenobarbital • IV dextrose, ventilation support as needed • Can result in hypoglycemia, hypotension, dysrhythmias • If goes > 1 hour, cerebral hypotension, breakdown of blood brain barrier, cerebral edema

17. Alterations in Cerebral Homeostasis • Cerebral edema • Most often caused by hypoxia, cerebral ischemia, fluid/electrolyte imbalance, meningitis, trauma • Peaks 36-48 hours after trauma • Leads to increased intracranial pressure • Blood vessels distorted, brain tissue displaced and eventually may herniate

18. Types of cerebral edema • Vasogenic (#1) • Increased permeability of of capillaries after injury • BB barrier damaged • Starts at site of injury, spreads to white matter of same side • Edema --> increased pressure -->local ischemia--> vasodilatation-->more edema

19. Cytotoxic (metabolic edema) • poisoning of active transport systems • Cells lose K, gain Na • Ischemic edema • Follows infarction • Both vasogenic and cytotoxic • Interstitial edema

20. Increased Intracranial Pressure • Cerebral edema #1 cause • Tumors, trauma (bleeding, edema), obstruction to CSF flow • Closed system, fluid is incompressible • Must have a decrease in contents to protect brain • CSF forced out of cranium • Vasoconstriction and compression of vessels provide early compensation

21. Progression of Pathophysiology • Reduced cerebral blood flow causes increased sympathetic activity • Vasoconstriction, increased BP • Brain becomes hypoxic and hypercapnic • Lowered LOC • Cheyne-Stokes breathing • Dilated, sluggish pupils • Bradycardia • Build up of CO2 leads to respiratory acidosis--> cerebral vasodilatation--> more edema • Herniation of brain compresses low P compartment

22. Clinical signs of increased ICP • Altered level of consciousness is most sensitive indicator • Classic triad • Headache, papilledema, vomiting (often projectile) • Hyperthermia, motor/sensory changes, altered speech, seizures • Coma when both hemispheres or brainstem stop functioning

23. ACQUIRED BRAIN INJURY Traumatic Injuries

24. Definition • Any insult caused by an external physical force may produce a diminished or altered state of consciousness can also result in the disturbance of behavioral or emotional functioning may be either temporary or permanent and cause partial or total functional disability or psychosocial maladjustment

25. Concussion • Most common type of traumatic brain injury • Caused when the brain receives trauma from an impact or a sudden momentum or movement change. • The blood vessels in the brain may stretch and cranial nerves may be damaged • Direct blows to the head, gunshot wounds, violent shaking of the head, or force from a whiplash type injury

26. Skull fracture, brain bleeding, or swelling may or may not be present • may or may not show up on a diagnostic imaging test • can cause diffuse axonal type injury resulting in permanent or temporary damage • blood clot in the brain can occur • It may take a few months to a few years for a concussion to heal

27. Diffuse Axonal Injury • Caused by shaking or strong rotation of the head, as with Shaken Baby Syndrome, or by rotational forces, such as with a car accident • Injury occurs because the unmoving brain lags behind the movement of the skull, causing brain structures to tear • tearing of the nerve tissue disrupts the brain’s regular communication and chemical processes

28. Shaken Baby Syndrome • Blood vessels between the brain and skull rupture and bleed • Accumulation of blood causes cerebral edema and increased intracranial pressure • Signs: Irritability, changes in eating patterns, tiredness, difficulty breathing, dilated pupils, seizures, and vomiting

29. Contusion • Bruise (bleeding) on the brain caused by direct impact • Signs are those of a mild concussion • Coup-Contrecoup Injury • Contusions that are both at the site of the impact and on the complete opposite side of the brain

30. Second Impact Syndrome (Recurrent Traumatic Brain Injury) • A person sustains a second traumatic brain injury before the symptoms of the first traumatic brain injury have healed • Loss of consciousness is not required • Second impact is more likely to cause brain swelling and widespread damage. • Long-term effects of recurrent brain injury can be muscle spasms, increased muscle tone, rapidly changing emotions, hallucinations, and difficulty thinking and learning.

31. Levels of brain injury • Assess using Glasgow Coma Scale • Provides an evaluation of initial level of injury • There may be no correlation between the initial Glasgow Coma Scale score and a person’s short or long term recovery, or functional abilities

32. Mild Traumatic Brain Injury (13-15) • Loss of consciousness is very brief, usually a few seconds or minutes, or does not occur—the person may be dazed or confused • Testing or scans of the brain may appear normal • Mild concussion, contusions

33. Symptoms of mild traumatic brain injury • Headache, Nausea • Memory problems, Decreased speed of thinking • Decreased concentration and attention span • Depression, anxiety, mood swings • Fatigue, Sleep disturbances, Irritability • Sensitivity to noise or light • Balance problems

34. Moderate Traumatic Brain Injury (9-12) • A loss of consciousness lasts from a few minutes to a few hours • All problems of mild trauma may last for days to weeks • Confusion lasts from days to weeks • Physical, cognitive, and/or behavioral impairments last for months or are permanent • Generally can make a good recovery

35. Severe Brain Injury (< 8) • Prolonged unconscious state or coma lasts days, weeks, or months • Categorized into subgroups • Coma • Vegetative State • Persistent Vegetative State • Minimally Responsive State • Akinetic Mutism • Locked-in Syndrome

36. Coma • State of unconsciousness from which the individual cannot be awakened • responds minimally or not at all to stimuli • initiates no voluntary activities • Cerebral cortex and lower areas are not working • If awaken, often left with permanent physical, cognitive, or behavioral impairments

37. Vegetative State • Arousal is present, but the ability to interact with the environment is not (cortex is gone) • Eye opening can be spontaneous or in response to stimulation • General responses to pain exist, such as increased heart rate, increased respiration, posturing, or sweating • Sleep-wakes cycles, respiratory functions, and digestive functions return • Persistent Vegetative State (PVS) is a term used for a Vegetative State that has lasted for more than a month

38. Minimally Responsive State • Severe traumatic brain injury, but no longer in a Coma or a Vegetative State • Primitive reflexes • Inconsistent ability to follow simple commands • An awareness of environmental stimulation • May last for years before some recovery

39. ACQUIRED BRAIN INJURIES Non-traumatic

40. Symptoms • Damage is diffuse, not focal, and at cellular level • mild, moderate, or severe impairments in one or more areas • cognition, speech-language communication; memory; attention and concentration; reasoning; abstract thinking; physical functions; psychosocial behavior; and information processing

41. Brain functionalities are more severely affected than in trauma • Cognitive impairment • Thinking skills, especially memory • Longer lengths of time spent in a vegetative state • Severe behavior problems- Psychosis, depression, restlessness, combativeness, hostility • Muscle movement disorders

42. Anoxic Brain Injury • Anoxic Anoxia- Brain injury from no oxygen supplied to the brain • Anemic Anoxia- Brain injury from blood that does not carry enough oxygen • Toxic Anoxia- Brain injury from toxins or metabolites that block oxygen in the blood from being used

43. Hypoxic Brain Injury Brain receives some, but not enough oxygen • critical reduction in blood flow or blood pressure. • Airway obstruction, near-drowning, strangulation, electrocution • Trauma to the head and/or neck or chest • Heart attack, stroke, arteriovenous malformation (AVM), aneurysm, intracranial surgery • carbon monoxide poisoning • Infectious disease, meningitis, intracranial tumors, metabolic disorders

44. Cerebral Vascular Disorders: Stroke • 3rd most common cause of mortality in US • increased risk for African Americans, women • major cause of disability in adults • Risk factors • smoking (50% increase in risk) • obesity, high BP, sleep apnea • DM (2.5-3.5 increase in risk) • impaired cardiac function (esp atrial fibrillation )

45. Definition • Sudden, nonconvulsive, focal loss of neuron activity • Neural insult from decreased blood flow • Thrombotic strokes • Embolic strokes • Hemorrhagic stroke

46. Thrombotic strokes • Attributed to local arteritis and atherosclerosis • Signs are usually slowly progressive (stroke in evolution) over several hours • Transient ischemic attacks are partial thrombotic strokes or the result of vessel spasm

47. Transient Ischemic Attacks • All neurologic deficits clear within 24 hours • Reversible ischemic neurologic deficits persist longer but do clear eventually • 80% of patients will have another episode within 1 year unless treated

48. Embolic strokes • Thrombus outside of brain breaks loose and migrates into cerebral vessels • L atrial fibrillation, valve disease, fat, air • Obstruction is usually at a bifurcation • Follow on strokes are common, because source of clot usually remains

49. Hemorrhagic stroke • Least common cause (10%) • Hypertension, aneurysms, bleeding into tumors, anticoagulation medication, head trauma

50. Signs and Symptoms • Sudden numbness or weakness—esp face, arm, leg, and usually one sided • Seeing double/change in visual field • Changed level of consciousness • Confusion to coma • Dizziness, stumbling, loss of balance/coordination • Severe headache with no known cause