Neurologic System Student Notes PDF

 QUESTIONS & REVIEW A & P: GROUP WORK Brain & Spinal Cord Cerebral hemodynamics Spinal Cord Injury (neurogenic & spinal shock, autonomic dysreflexia) CSF & ICP Delerium & Dementia...

 QUESTIONS & REVIEW A & P: GROUP WORK Brain & Spinal Cord Cerebral hemodynamics Spinal Cord Injury (neurogenic & spinal shock, autonomic dysreflexia) CSF & ICP Delerium & Dementia Intracerebral hypertension Brain Injury (CVA, TBI) (cerebral edema, ICP ) Seizures QUESTIONS & REVIEW & GROUPS CEREBRAL HEMODYNAMICS MONROE-KELLIE DOCTRINE: The brain, the blood, & the cerebrospinal fluid exist within the rigid skull. An increase in any one of these components will increase intracranial pressure (ICP). If the volume of one increases, the volume of another has to decrease in order to maintain a normal ICP. Brain = 80% Blood = 10% CSF = 10%  CEREBROSPINAL FLUID Intracranial & spinal cord structures float in clear, odorless cerebrospinal fluid (CSF) Provides the buoyancy to cushion the brain and spinal cord during jolts and blows that would otherwise cause injury as they impact the bony structures encasing them. Approximately 125 – 150cc of CSF circulates around the brain & spinal cord at any given time with 75ccs specifically circulating in the intracranial compartment.. Produced by the choroid plexus (collections of blood vessels covered by highly specialized cells) located in the lateral, third, & fourth ventricles of the brain. The ventricles are hollow spaces in the brain whose walls are formed by surrounding structures  CSF CSF exerts pressure on brain and spinal cord CSF flow is a result of a pressure gradient between the arterial system and the CSF filled cavities. CSF flows from lateral ventricles  third ventricle  through cerebral aqueduct  fourth ventricle  pontine cisterns or cerebromedullary cistern & finally  into the subarachnoid spaces of the brain & spinal cord. **A cistern is any opening of the subarachnoid space created by a separation of the arachnoid and pia mater.  CSF The CSF does not accumulate but rather is constantly reabsorbed into the venous circulation through the arachnoid villi. Arachnoid villi protrude from the arachnoid space through the Dura mater and lie within the blood flow of the venous sinuses. CSF is reabsorbed by means of a pressure gradient between the arachnoid villi and the cerebral venous sinuses. -The villi act as one-way valves that open at a pressure gradient of 5mmHg and then close so not allow flow back into the subarachnoid space. -Flow stops when the pressure gradient is < 5 mmHg. -CSF ultimately drains into the jugular system for return to the heart. -CSF is continuously secreted and so, is reliant on the patency of the arachnoid villi for normal flow to occur. **Obstruction of the arachnoid villi results in an accumulation of CSF & an LUMBAR PUNCTURE Samples of CSF can be taken through a lumbar puncture into the space between the third & fourth lumbar vertebrae or from an intraventricular catheter. Evaluation of a CSF  Xanthochromia – discoloration caused by the breakdown of RBCs which can be sample: detected 3 hrs after a SAH  WBC - 0-5 cells/mm3 is normal if agranulocytes, elevation is seen in meningitis, intracranial infections, intracranial and spinal tumors, multiple sclerosis  Protein – 15-45mg/100 ml is normal, elevations are seen in tumors, infections, and hemorrhages  Glucose – 60-100 mg/ 100 ml or 80% of blood glucose is normal, less than normal levels indicates the presence of glycolytic substances such as bacteria. CEREBRAL HEMODYNAMICS MONROE-KELLY DOCTRINE: The brain, the blood, & the cerebrospinal fluid exist within the rigid skull. An increase in any one of these components will increase intracranial pressure (ICP). If the volume of one increases, the volume of another has to decrease in order to maintain a normal ICP. Brain = 80% Blood = 10% CSF = 10%  INTRACRANIAL PRESSURE Intracranial pressure (ICP = 5-15mmHg) can be increased by: Increased Brain volume: Tumor, hematoma, edema, abscess, infection Increased Blood volume: Increased arterial flow, decreased venous drainage Increased CSF volume: Hydrocephalus from increased production, obstruction to flow The brain structures have some ability to displace blood & CSF when ICP rises however when the ability to autoregulate becomes overwhelmed the ICP will more rapidly increase until the brain herniates into the brainstem with inevitable brain death resulting. CEREBRAL EDEMA CEREBRAL EDEMA is the accumulation of fluid in brain tissue that increases pressure within the cranial vault. VASOGENIC: Increased capillary permeability leading to the movement of water & proteins from the intravascular space to the extravascular space. The blood brain barrier is broken down by direct injury, tumor or local inflammation. CYTOTOXIC: Neuronal, glial & endothelial cellular swelling 20 loss of N + - K+ pump function usually as a result of ischemia of these cells. The blood brain barrier remains intact. INTERSTITIAL: Increased fluid in the periventricular white matter caused by increased CSF hydrostatic pressure as in hydrocephalus.  CEREBRAL AUTOREGULATION Stage I: Vasoconstriction to decrease blood flow into the brain Stage II: The ICP becomes too high to compensate with vasoconstriction of cerebral arteries. Systemic HTN occurs in an attempt to force an adequate amount of blood upward against the opposing ICP Stage III: The ICP rises to almost equal arterial pressure leading to brain tissue ischemia further causing inflammation & edema. ICP begins to rise rapidly. Autoregulation fails. Stage IV: Increased pressure in the cranial vault causes the brain to herniate. This leads to more ischemia, obstructive hydrocephalus until ICP = systemic blood pressure & cerebral blood flow ceases. CLINICAL SIGNS & SYMPTOMS OF INCREASED ICP  ALTERED DATA PROCESSING DELIRIUM vs. DEMENTIA ALZHEIMER’S DISEASE was first diagnosed in 1906 by Dr. Alzheimer when he noted distinctive plaques & neurofibrillary tangles in the brain histology of one of his patients. Leading cause of sporadic older age (>65) dementia Rare cases of early age (30-40) familial cases exist Currently 55 million cases  ALTERED DATA PROCESSING: ALZHEIMER’S DISEASE Pathophysiology theoretically related to distinct brain findings in people with Alzheimer’s 1. EXTRANEURONAL ẞ-Amyloid PROTEIN PLAQUES ẞ-Amyloid protein is normally found between neurons and plays an undefined role in nerve cell development. Excess amounts cluster to form plaques believed to be a result of an enzyme deficiency or a genetic mutation affecting over-production of the protein. 2. INTRANEURONAL TAU PROTEIN NEUROFIBRILLARY TANGLES Tau protein is normally found within neurons where it contributes to the formation of the supportive microtubules that make up the cytoskeleton. A lack of enzyme or a genetic defect leads to overproduction of tau protein which cluster to form neurofibrillary tangles. 3. ACETYCHOLINE DEFICIT  ALTERED DATA PROCESSING: ALZHEIMER’S DISEASE Most likely a combination or relationship between the 3 proposed pathophysiological causes of Alzheimer’s lead to: Neuron death & inflammation Brain atrophy particularly in the entire cortex & hippocampus Enlargement of ventricles *The severity of brain plaques and neurofibrillary tangles do not correlate to symptoms STAGES OF ALZHEIMER’S Stage 1 Normal, no deficits Stage 2 Mild cognitive deficits, forgetting words, misplacing items Stage 3 Mild confusion which is purposefully hidden from others, little retention of what has just been said or read, difficulty planning & organizing Stage 4 Inability to do financial work, inability to recall what was just learned or to perform a task that requires pre-learned steps such as driving Stage 5 Requires assistance, cannot recall own address, phone number etc Stage 6 Lacks awareness of past and present, unable to converse, perform ADLs, unable to recall loved one’s names but recognizes them as familiar Stage 7 Limited speech, movements such as standing, sitting, feeding affected, inability to recognize hunger, thirst, susceptibility to secondary complications. This can occur as progression over 12 years or more  ALZHEIMER’S MANAGEMENT Initially anticholinesterase agents were used to treat people with Alzheimer’s however they offer only a transient change and no true alteration in the progression of the disease New treatments are looking to target critical steps in the formation of plaques and tangles however remain in experimental stages. Management currently involves environmental management, memory aids, & exercises to maintain current cognitive functions for as long as possible. FOCAL BRAIN INJURY SYMPTOMS BY LOCATION Impaired blood flow through a specific cerebral artery also dictates the area of injury and associated symptoms CEREBRAL INJURY Initial injuries of the brain are often not what causes permanent deficits. Secondary injury; ischemia, edema and hyperemia lead to increased intracranial pressure and brain cell death. Goal of treatment is to minimize secondary injury and salvage as many brain cells as possible after injury. The extent of cellular damage correlates to functional outcome.  ALTERATIONS IN THE CENTRAL NERVOUS SYSTEM Traumatic Brain Injury (TBI) is the acute loss of brain function caused by an external force. Closed Head Injury: The brain suffers an impact either from the head striking a hard surface or a rapidly moving object striking the head. The dura is uninterrupted. Open Head Injury: A penetrating trauma in which the dura is interrupted, exposing brain tissue to the environment.  FOCAL BRAIN INJURY: CONTUSION FOCAL BRAIN INJURY refers to injury at the point of impact and rebound sites CONTUSION: Injured blood vessels within the affected focal brain tissue. Areas of hemorrhage, infarction, necrosis, & edema exist within the contused tissue. Symptoms vary with severity & may include: LOC 24 hours, widespread deficits with intact brainstem function SEVERE AXONAL INJURY: Impaired brainstem function for days, severe deficits & 78% mortality  PRIMARY SECONDARY INJURY (Lasting tissue changes)  CEREBROVASCULAR ACCIDENTS CVAs are classified by the underlying pathology Ischemic Hemorrhagic Thrombotic Embolic Global Hypoperfusion / Anoxia Non-traumatic Intracerebral Hemorrhage Cerebral Distant thrombus Shock states/hypotension Intracranial, Subarachnoid thrombosis fragment  ISCHEMIC STROKE No matter the classification/etiology, the initially injured tissue is surrounded by tissue at risk. The focus of treatment is to restore perfusion as quickly as possible & maintain optimal perfusion in order to salvage as many neurons. Thrombolytic therapy Clot Retrieval TPA MERCI procedure  HEMORRHAGIC STROKE Hemorrhage can be spontaneous, can occur when an ischemic stroke has a hemorrhagic conversion, or a vascular malformation occurs. The increased pressure caused by the blood and the secondary tissue injury below the blood is as detrimental as the focal ischemia caused by the interrupted blood flow. Aneurysm AV malformation  SEIZURE DISORDERS A SEIZURE is an abrupt excessive discharge of electrical impulses from the cortical neurons. It is the result of a change in neuronal environment that disturbs the balance between the excitation & inhibition of impulses. Excitation Inhibiti on → SEIZURES FOCAL VS. GENERALIZED PARTIAL (FOCAL) SEIZURES: Hypersynchronous electrical discharges usually originate from focal cortical neurons in one hemisphere and remain in that hemisphere. GENERALIZED SEIZURES: Hypersynchronous electrical discharges originate in multiple subcortical foci in both hemispheres spontaneously. TYPES OF SEIZURES PARTIAL SEIZURE GENERALIZED SEIZURE CAUSES OF SEIZURES GROUP WORK: PART II Part I (all groups): What is the pathophysiology of a A 60-year-old woman with no known spinal cord injury? past medical history presents to the What would you expect to find emergency department after with her neurological exam? sustaining a fall off a 20-foot ladder What could happen if she while cleaning her gutters. A CT scan of develops significant swelling in her cervical spine shows C6 subluxation with spinal cord injury. She is unable to her spinal cord? move her arms and legs. What are the possible treatment options?  SPINAL CORD INJURY SPINAL CORD INJURY results from both primary and secondary injury just as in brain tissue. Increased pressure within the canal acts in the same devastating manner as in the cranial vault. LEVEL OF INJURY: SENSORY & MOTOR DEFICITS MYOTOMES DERMATOMES PARTIAL SPINAL CORD INJURY  NEUROGENIC VS. SPINAL SHOCK SPINAL SHOCK is a complete loss of reflexes and flaccidity below the level of injury. This may last for days to 3 months at which time the person develops hyper-reflexia and spasms. NEUROGENIC SHOCK occurs in cervical & upper thoracic injuries. Sympathetic tone is lost. Parasympathetic system / vagus nerve is unopposed resulting in bradycardia, hypotension, & hypothermia  AUTONOMIC DYSREFLEXIA Injuries above T6 may cause the life-long threat of a fatal hypertensive crisis. Irritation below the level of injury from pain, a full bladder or bowel initiates the response. Treatment is to eliminate the stimuli and cautiously administer short acting anti-hypertensives other than beta blockers GROUP WORK: PART III Part III (all groups): Explain the pathophysiology A 45-year-old man with a past medical history of polysubstance use is found of intracranial hypertension. unresponsive outside of his home. He is What are the symptoms? given Narcan in the ambulance without improvement. A cranial CT scan is What are potential treatment performed which shows a large intracerebral hemorrhage with mass options? effect and midline shift. You are concerned with elevated intracranial hypertension. ICH: