Week 2 Neuro Readings PDF

Week 2 readings **Canadian Clinical Skills: Essentials Collection** - Assessing the Neurologic System: Mental Status and Cranial Nerves - Assessing the Neurologic System**:** Motor and Sensory Systems Key terms to know: +-----------------------+-----------------------+----------------------...

Week 2 readings **Canadian Clinical Skills: Essentials Collection** - Assessing the Neurologic System: Mental Status and Cranial Nerves - Assessing the Neurologic System**:** Motor and Sensory Systems Key terms to know: +-----------------------+-----------------------+-----------------------+ | - Acquired Brain | Diffuse Axonal | Neurological | | Injury | Injury | Recheck | | | | | | Aphasia | -widespread damange | Nuchal Rigidity | | | to axons d/t rapid | | | -cant understand, | acceleration or | -stiffness/difficulty | | process or produce | deceleration forces. | bending neck | | speech | | | | | Encephalitis | Paralysis | | Ataxia | | | | | -inflammation of | Post-concussion | | -lack of voluntary | brain tissue | syndrome | | muscle coordination. | | | | Balance, gait, fine | Epidural hematoma | -sx weeks/months | | motor control | | after. | | affected | -blood between skull | | | | and dura mater | Ptosis | | Atrophy | | | | | Glasgow Coma Scale | -drooping of upper | | Brain Abscess | (GCS | eyelid | | | | | | Canadian | Intracranial | Romberg Sign | | Neurological Scale | Pressure (ICP) | | | | | -test where person | | Cerebral Edema | Intraparenchymal or | stands with feet | | | intracerebral | together +eyes | | Chronic traumatic | hemorrhage | closed. + sign is | | Encephalopathy (CTE) | | when they cant do it. | | | Meningitis | | | -accumulation of tau | | Seizures | | protein in brain from | Mini Mental State | | | repeated head injury | Examination | Strabismus | | | | | | Concussion | Montreal Cognitive | -eyes point in diff. | | | Assessment | directions | | Contusion | | | | | Muscle Paresis | Subdural hematoma | | -bruise that results | | | | from impact. Doesn't | | Tremor | | break skin | | | +-----------------------+-----------------------+-----------------------+ \*\*need to know different types of seizures **Required Readings** **Davis, G. A. et al. (2017). Concussion in Sport (SCAT5). *BR J Sports Med,* 1-8 http://www.sportphysio.ca/wp-content/uploads/SCAT-5.pdf**  **Purpose of SCAT5**: - The SCAT5 (Sports Concussion Assessment Tool 5th Edition) is designed to evaluate athletes suspected of having a concussion. It provides a comprehensive assessment to determine the presence and severity of a concussion.  **Components of SCAT5**: - **Symptom Checklist**: Assesses the severity and number of symptoms experienced by the athlete. - **Physical Examination**: Includes tests of balance, coordination, and cognitive function. - **Standardized Assessment of Concussion (SAC)**: Evaluates cognitive functions such as orientation, immediate memory, and concentration. - **Neurological Examination**: Checks for any neurological deficits.  **Administration Timing**: - **Pre-Season Baseline Testing**: Ideally, athletes should complete a baseline SCAT5 assessment before the start of the sports season for comparison in case of a suspected concussion. - **Post-Injury Assessment**: The SCAT5 should be administered as soon as possible after a suspected concussion and may need to be repeated periodically to monitor recovery.  **Clinical Decision-Making**: - **Immediate Removal**: Athletes suspected of having a concussion should be immediately removed from play and not return until cleared by a healthcare professional. - **Follow-Up**: Continuous monitoring and follow-up assessments are crucial for proper management and safe return to play.  **Assessment and Management**: - **Guidelines for Management**: The SCAT5 provides guidelines for managing concussions, including physical and cognitive rest, and a stepwise approach to return-to-play.  **Validation and Reliability**: - The SCAT5 is an updated tool based on research and clinical experience, aiming to improve the accuracy and reliability of concussion assessments in sports.  **Application**: - Used by healthcare professionals, including team physicians, athletic trainers, and other medical personnel, to assess and manage sports-related concussions. **Johnston, S.L. & Keller, K. (2023). Nursing Management: Acute Intracranial Conditions. In J. Tyerman & S. L. Cobbett (Eds.), *Lewis's medical-surgical nursing in Canada: Assessment and management of clinical problems* (5th ed., pp. 1453-1484). Elsevier Canada.** - ** Read only: pages 1453-1474 (\*up to brain tumours)** - **Factors influencing ICP under normal circumstances:** - Blood pressure (BP) - Cardiac function - Intra-abdominal and intrathoracic pressure - Body position - Temperature - Blood gases, particularly carbon dioxide (CO2) levels - **Impact on ICP:** - The extent of ICP increase or decrease depends on the brain's ability to accommodate changes. - **Types of injury:** - **Primary injury:** - Occurs at the time of injury (e.g., motor vehicle accident, blunt-force trauma) - Results in displacement, bruising, or damage of the brain components. - **Secondary injury:** - Results from hypoxia, ischemia, hypotension, edema, or increased ICP following the primary injury. - Can occur hours to days after the initial injury. - A primary concern in managing brain injury. - **Nursing management:** - Must include management of secondary injury and increased ICP. - **ICP measurement:** - Can be measured in: - Ventricles - Subarachnoid space - Subdural space - Epidural space - Brain tissue - Normal ICP range: 5 to 15 mm Hg - Sustained pressure greater than 20 mm Hg is considered increased and requires treatment.Bottom of Form  **Normal Compensatory Adaptations:** - Intrinsic mechanisms resist increases in intracranial pressure (ICP). - Major compensatory mechanism: Changes in cerebrospinal fluid (CSF) volume. - CSF displaced to spinal subarachnoid space or basal cisterns. - Alterations in CSF production and absorption rates. - Alterations in intracranial blood volume: - Compression of cerebral veins and dural sinuses. - Regional cerebral vasoconstriction or dilation. - Changes in venous outflow. - Brain tissue volume compensates: - Distension of dura or compression of brain tissue. - Initially, increased volume does not raise ICP due to compensatory mechanisms. - Over time, compensatory mechanisms become exhausted, leading to increased ICP, neuronal compression, and ischemia.  **Cerebral Blood Flow (CBF):** - Amount of blood passing through 100 grams of brain tissue per minute. - Approximately 50 mL/min/100 g or 750 mL/min in adults. - Brain uses 20% of body's oxygen and 25% of glucose despite its small weight.  **Autoregulation of Cerebral Blood Flow:** - Brain regulates blood flow in response to metabolic needs despite systemic BP fluctuations. - Autoregulation maintains constant blood flow and cerebral perfusion pressure. - Fails in extreme hypotension (MAP \< 50 mm Hg) or hypertension (MAP \> 150 mm Hg).  **Other Factors Affecting CBF:** - **Carbon Dioxide (PaCO2):** - Increased PaCO2 dilates cerebral vessels, increases CBF. - Decreased PaCO2 constricts vessels, decreases CBF. - **Oxygen (PaO2):** - PaO2 \< 50 mm Hg causes vessel dilation, increases CBF. - Low PaO2 leads to anaerobic metabolism and lactic acid accumulation. - **Hydrogen Ions (Acidosis):** - Increased acidity leads to further vasodilation and attempts to increase CBF. - Severe hypoxia and acidosis can disrupt autoregulation and compensatory mechanisms.  **Global and Regional Factors Affecting CBF:** - **Global:** - Affected by cardiac or respiratory arrest, systemic hemorrhage, diabetic coma, encephalopathies, infections, and toxicities. - **Regional:** - Affected by trauma, tumors, cerebral hemorrhage, or stroke. - Loss of autoregulation results in CBF being influenced directly by systemic BP, PaCO2 levels, or catecholamine levels. - Cerebral perfusion pressure (CPP) can reflect changes in CBF. - **Cerebral Perfusion Pressure (CPP):** - CPP is the pressure needed to ensure adequate brain tissue perfusion (CPP = MAP − ICP). - To improve inadequate CPP, either decrease ICP or increase MAP. - Normal CPP ranges from 70 to 100 mm Hg; at least 50 to 60 mm Hg is needed for adequate cerebral perfusion. - CPP below 50 mm Hg is associated with cerebral ischemia; below 30 mm Hg is life-threatening. - Autoregulation maintains CBF and perfusion pressure, but it fails if CPP is too low or high. - CPP does not always reflect perfusion in all brain areas; localized swelling may require a higher CPP. - **Pressure-Volume Relationship:** - Depicted by the pressure--volume curve, which is affected by brain compliance (expandability). - Low compliance means small volume increases cause significant ICP increases. - **Stages of Increased ICP:** - **Stage 1:** High compliance, no ICP increase with volume change. - **Stage 2:** Decreasing compliance, risk of increased ICP with volume increase. - **Stage 3:** Low compliance, small volume changes lead to significant ICP increases and symptoms. - **Stage 4:** Lethal ICP levels, risk of hypoperfusion, brain herniation, and death. - **Increased Intracranial Pressure (ICP):** - Results from increases in brain tissue, blood, or CSF. - Elevated ICP diminishes CPP, raising the risk of brain ischemia, infarction, and herniation. - **Mechanisms:** - **Brain Tissue:** Neoplasm, contusion, abscess, cerebral edema. - **Blood Volume:** Hematomas, hemorrhages, metabolic factors (e.g., CO2, O2), vascular anomalies. - **CSF Volume:** Tumors secreting CSF, hydrocephalus. - Increased ICP can cause hypercapnia, acidosis, impaired autoregulation, and systemic hypertension. - Sustained or rapidly increasing ICP may lead to brainstem compression, herniation, and severe outcomes like respiratory arrest or death. - A diagram of a flowchart Description automatically generated -  **Vasogenic Cerebral Edema:** - **Type:** Most common, primarily affects white matter. - **Cause:** Changes in endothelial lining of cerebral capillaries increase permeability. - **Mechanism:** Leakage of macromolecules into extracellular space creates osmotic gradient, drawing water from intravascular to extravascular space. - **Insults:** Brain tumors, head trauma, abscesses, toxins. - **Influences:** Systemic BP, site of brain injury, extent of blood-brain barrier defect. - **Symptoms:** Range from headache and focal neurological deficits to disturbances in consciousness, including coma. - **Note:** Headaches may progress rapidly to severe conditions like coma or death; vigilant assessment is crucial. -  **Cytotoxic Cerebral Edema:** - **Type:** Affects grey matter. - **Cause:** Disruption of cell membrane integrity, leading to hypoxia, sodium depletion, or SIADH. - **Mechanism:** Fluid and protein shift into cells, causing cellular swelling and loss of function. -  **Interstitial Cerebral Edema:** - **Cause:** Periventricular diffusion of ventricular CSF, uncontrolled hydrocephalus, or systemic water excess (hyponatremia). - **Mechanism:** Fluid moves into cells to equilibrate with hypo-osmotic interstitial fluid. - **Clinical Manifestations of Increased ICP:** - **Change in Level of Consciousness (LOC):** - Sensitive indicator of neurological status. - Impaired cerebral blood flow (CBF) affects the reticular activating system (RAS) and cortical function. - Range from subtle changes (e.g., confusion, decreased attention) to profound unconsciousness or coma. - EEG may show decreased neuronal activity. - **Decrease in Motor Function:** - Contralateral hemiparesis or hemiplegia depending on injury location. - Motor responses to stimuli may include localization or withdrawal. - Abnormal posturing: - **Decorticate Posturing:** Internal rotation, adduction, flexion of arms; extension of legs. - **Decerebrate Posturing:** Stiff, extended arms, hyperpronated; extended legs, plantar flexion of feet. - **Headache:** - Continuous pain due to compression of intracranial structures. - May worsen with straining, agitation, or movement. - **Vomiting:** - Often without preceding nausea. - Related to pressure on the vomiting center in the medulla. - **Changes in Vital Signs:** - **Cushing's Triad:** Increasing systolic pressure, bradycardia, irregular respiration. - Indicates brainstem compression and is a medical emergency. - Changes in body temperature may occur due to hypothalamic pressure. - **Ocular Signs:** - Compression of oculomotor nerve (CN III) can cause: - Unilateral pupil dilation, sluggish or no light response, inability to move the eye upward, ptosis. - Fixed, unresponsive dilated pupil is an emergency indicating brain herniation. - Possible involvement of other cranial nerves (e.g., optic (CN II), trochlear (CN IV), abducens (CN VI)): - Signs include blurred vision, diplopia, and changes in eye movements. - Central herniation may show sluggish but equal pupil responses; lateral herniation affects the uncus and is more severe. - **Medication Therapy for Managing Increased ICP:** - **Mannitol (Osmitrol):** - **Type:** Osmotic diuretic, administered intravenously. - **Mechanism:** Reduces ICP through plasma expansion and osmotic effect, lowering total brain fluid content. - **Monitoring:** Requires close monitoring of fluid and electrolyte balance. Watch for increased serum sodium levels and osmolality. - **Medication Alert:** - Risk of fluid shift, fluid overload, and pulmonary congestion. - May crystallize at lower temperatures; administer with a filter. - **Hypertonic Saline:** - **Purpose:** Reduces swelling, improves cerebral blood flow (CBF), and draws water out of brain tissue. - **Monitoring:** Requires close monitoring of blood pressure (BP) and serum sodium levels due to potential fluid volume excess. - **Effectiveness:** Often more effective as a first-line treatment for elevated ICP compared to mannitol. - **Corticosteroids (e.g., Dexamethasone):** - **Use:** Treats vasogenic edema surrounding tumors and abscesses; limited value in head injuries. - **Mechanism:** Stabilizes cell membranes, inhibits prostaglandin synthesis, and improves CBF and autoregulation. - **Complications:** Hyperglycemia, increased infection risk, gastrointestinal (GI) bleeding, hyponatremia. - **Monitoring:** Regular monitoring of fluid intake, sodium, and glucose levels. Co-administer antacids or H2-receptor blockers to prevent GI ulcers. - **Sedation and Analgesia:** - **Agents:** Propofol (Diprivan) for sedation. - **Purpose:** Manage elevated ICP by reducing cerebral metabolism. - **High-Dose Barbiturates (e.g., Pentobarbital Sodium \[Somnotol\]):** - **Use:** For ICP refractory to other treatments. - **Mechanism:** Dampen environmental stimuli, decrease cerebral metabolism, and reduce ICP. - **Monitoring:** Requires monitoring of ICP, blood flow, EEG, and metabolism. Risk of hypotension. - **Anticonvulsants (e.g., Phenytoin \[Dilantin\]):** - **Purpose:** Prevent seizures, which can further increase ICP. **Neurological Assessment Summary:** - **Pupillary Response:** - **Comparison:** Check size, movement, and response of pupils. - **Effects of Increased ICP:** - Compression of the oculomotor nerve causes ipsilateral pupil dilation. - Progressive ICP increase leads to bilateral pupil dilation. - **Testing:** - Measure pupil size in millimeters. - Use a penlight to assess direct and consensual constriction. - Sluggish or fixed pupils indicate potential increased ICP or other issues (e.g., CN III injury, eye surgery, atropine, mydriatic drops). - **Cranial Nerve Assessment:** - **Eye Movements:** - CNs III, IV, VI control eye movements; assess in awake patients or use reflex tests (oculocephalic, oculovestibular) in unconscious patients. - **Corneal Reflex:** - Tests CNs V and VII; absence requires eye care to prevent corneal abrasion. - **Motor Function:** - **Awake Patients:** - Test hand strength by squeezing. - **Palmar Drift Test:** Patient raises arms with palms up; drifting inward indicates weakness. - Assess lower extremities by asking the patient to lift feet or bend knees. - **Unconscious/Uncooperative Patients:** - Observe spontaneous movements or responses to pain stimuli. - Assess resistance during passive range-of-motion exercises. - **Vital Signs:** - **Routine Measurement:** BP, pulse, respiratory rate, and temperature. - **Cushing's Triad:** Increased BP with widening pulse pressure, bradycardia, and irregular respiration suggest severe increased ICP and potential cerebral herniation. - **Respiratory Patterns:** Specific patterns may indicate severe ICP elevation. **Types of Head Injuries: Summary** - **Scalp Lacerations:** - **Description:** Minor head trauma involving tears in the scalp. - **Complications:** Profuse bleeding due to scalp\'s many blood vessels and risk of infection. - **Skull Fractures:** - **Types:** Linear, depressed, simple, comminuted, compound, closed, or open. - **Symptoms:** Headache, weakness, loss of balance, vision or hearing changes, dizziness. - **Specific Types:** - **Basilar Skull Fracture:** Characterized by Battle sign (postauricular ecchymosis) and periorbital ecchymosis (raccoon eyes). May involve CSF leakage (rhinorrhea or otorrhea) and cranial nerve damage. - **Complications:** Intracranial infections, hematoma, meningeal and brain tissue damage. - **Diffuse Injury:** - **Concussion:** Mild traumatic brain injury causing transient neural disruption and changes in LOC. Symptoms include temporary loss of consciousness, memory loss, and confusion. - **Diffuse Axonal Injury (DAI):** Widespread axonal damage primarily in subcortical white matter, basal ganglia, thalamus, and brainstem. Causes decreased LOC, increased ICP, and global cerebral edema. - **Focal Injury:** - **Contusions:** Bruising of brain tissue, often at site of skull fracture (coup) and opposite side (contrecoup). Can involve hemorrhage and evolving contusions leading to poor prognosis. - **Lacerations:** Tearing of brain tissue, often associated with depressed fractures and penetrating injuries. Severe tissue damage, often not repairable. - **Testing for CSF Leak:** - **Methods:** - **Glucose Testing:** Dextrostix or Tes-Tape to detect glucose in fluid. - **Halo Sign:** Blood coalesces with a yellowish ring of CSF on a white pad. - **Severity Classification:** - **Mild TBI:** GCS score of 13-15, may include concussions. - **Moderate TBI:** GCS score of 9-12. - **Severe TBI:** GCS score of 3-8. - **General Considerations:** - **Chronic Issues:** Repeated concussions can lead to chronic traumatic encephalopathy (CTE) and long-term brain degeneration. - **Recurrent Injuries:** Increased risk with previous concussions and may affect recovery. **Complications of Head Injuries: Summary** 1. **Epidural Hematoma:** - **Description:** Blood collection between the dura mater and skull, often from a torn artery. - **Characteristics:** Can lead to rapid compression of the brain, especially if the bleeding is under high pressure. - **Symptoms:** Brief loss of consciousness followed by a lucid interval, headache, nausea, vomiting, and possible decrease in LOC. - **Treatment:** Immediate surgical intervention to prevent cerebral herniation. 2. **Subdural Hematoma:** - **Description:** Blood collection between the dura mater and the arachnoid layer, usually from injury to the brain's parenchymal vessels or bridging veins. - **Types:** - **Acute:** Develops within 48 hours of injury, with symptoms similar to increased ICP (decreasing LOC, headache). - **Subacute:** Occurs within 2 to 14 days of injury, with potential gradual enlargement of the hematoma. - **Chronic:** Develops over weeks to months, often in older adults or those with brain atrophy. Symptoms may be mistaken for other conditions such as dementia. - **Symptoms:** Somnolence, confusion, lethargy, memory loss. 3. **Intraparenchymal Hematoma (Intracerebral Hematoma):** - **Description:** Blood collection within the brain tissue itself, often in the frontal and temporal lobes. - **Characteristics:** Occurs from the rupture of intracerebral vessels, with outcomes depending on the size and location of the hematoma. 4. **Traumatic Subarachnoid Hemorrhage:** - **Description:** Bleeding into the subarachnoid space from damaged superficial vascular structures. - **Complications:** Can lead to cerebral vasospasm and decreased cerebral blood flow (CBF), increasing the risk of ischemic damage. **Diagnostic and Interventional Care:** - **Diagnostic Tools:** - **CT Scan:** Preferred for rapid diagnosis of craniocerebral trauma. - **MRI Scan:** More sensitive for detecting small diffuse axonal injury lesions. - **Transcranial Doppler:** Measures CBF velocity. - **Cervical Spine Radiography:** Assesses potential concomitant cervical spine injury. - **Management:** - **Observation and ICP Management:** For concussion and contusion. - **Surgical Intervention:** Needed for significant skull fractures, large subdural and epidural hematomas, and in cases of neurological impairment. Methods include craniotomy, craniectomy, and burr-hole approaches. **Key Points:** - **Epidural Hematoma:** Requires rapid surgical intervention to avoid severe outcomes. - **Subdural Hematoma:** Varies in development speed; chronic cases may be missed in older patients. - **Intraparenchymal Hematoma:** Significant for its impact on patient outcomes based on size and location. - **Traumatic Subarachnoid Hemorrhage:** Can lead to serious complications including vasospasm and ischemia. **Acute Intervention and Management of Head Injuries** **At the Scene of the Accident:** - **Goal:** Maintain cerebral oxygenation and perfusion, prevent secondary cerebral ischemia. - **Initial Care:** - Ensure airway, breathing, and circulation are stable. - Immobilize the patient to prevent further injury. - Monitor neurological status frequently, including GCS (Glasgow Coma Scale). **Hospital Management:** - **Neurological Monitoring:** - Frequent assessments for changes in level of consciousness (LOC), motor strength, and pupillary response. - Calm, supportive communication with both patient and caregivers is essential to manage anxiety and confusion. - **Eye Care:** - Address corneal reflex loss with lubricating drops, eye taping, or suturing if necessary. - Periorbital ecchymosis and edema can be treated with cold and warm compresses. - Diplopia may be managed with an eye patch. - **Temperature Regulation:** - Control hyperthermia to prevent increased cerebral metabolic rate and ICP. Aim for a normothermic range (36°C to 38°C). - **CSF Leak Management:** - Elevate the head of the bed to reduce CSF pressure. - Avoid placing dressings in the nasal cavity or ear canal. - Avoid sneezing, nose-blowing, and nasotracheal suctioning to prevent meningitis. - **General Care:** - Manage bladder and bowel function, skin care, and prevent infection. - Address nausea with antiemetics and headaches with acetaminophen or codeine. - Be prepared for potential urgent surgery (e.g., burr-hole, craniotomy) if the condition worsens. **Post-Acute Care:** - **Rehabilitation:** - Transition to acute rehabilitation once stabilized to address motor and sensory deficits, cognitive and communication issues. - Management may include nutritional support, bowel and bladder care, spasticity management, and addressing post-traumatic seizures. - **Cognitive and Emotional Support:** - Anticipate changes in behavior, concentration, memory, and mood swings. - Provide family support, help them understand the patient's condition, and guide them in realistic expectations and interactions. - **Discharge Planning:** - Provide specific post-discharge instructions: no alcohol, no driving, no hazardous activities, and no unsupervised smoking. - Offer referrals for community support and financial aid as needed. **Family Support:** - **Preparation and Education:** - Prepare the family for the patient's recovery process, which may take weeks to months. - Provide guidance on managing expectations and adapting to the patient's evolving condition. **Emergency Considerations:** - **Preoperative and Postoperative Care:** - Ensure any coexisting life-threatening conditions are addressed. - Monitor closely for signs of deterioration requiring potential emergency surgery. Top of Form Bottom of Form Top of Form Bottom of Form Top of Form Bottom of Form Top of Form Bottom of Form Top of Form Bottom of Form Top of Form Bottom of Form **Ouellette, D., Plueger, M.D. & Roberts, D. (2023). Nursing Management: Chronic Neurological Problems. In J. Tyerman & S. L. Cobbett (Eds.), *Lewis's medical-surgical nursing in Canada: Assessment and management of clinical problems* (5th ed., pp. 1511-1540). Elsevier Canada.** - **Read only: pages 1516-1523** (\*seizure disorder and epilepsy section) **Seizure Disorder Overview** **Seizure disorder**, also known as epilepsy, involves recurring seizures due to abnormal electrical discharges in the brain. Seizures can disrupt normal brain function and are categorized into various types based on their onset and manifestations. **Etiology and Pathophysiology** Seizures can result from a range of underlying conditions: - **Idiopathic Seizures:** Approximately 50% of epilepsy cases have no known cause. - **Metabolic Disturbances:** Conditions such as electrolyte imbalances, hypoglycemia, and alcohol withdrawal can provoke seizures. - **Structural Lesions:** Tumors, trauma, and vascular disease are common causes in adults. - **Systemic Disorders:** Heart, liver, and kidney diseases can contribute to seizures. **Genetic Factors** may also play a role, with some families showing a predisposition to seizures. **Pathophysiology**: - Seizures often begin in a localized area of the brain but can spread. - Abnormal neuron firing is central to seizure activity. - Changes in astrocytes and the presence of abnormal neural antibodies may also be involved. **Clinical Manifestations** Seizures are categorized based on their onset and progression: 1. **Generalized Onset Seizures:** Affect both sides of the brain from the beginning. - **Tonic--Clonic Seizures:** Involve stiffening (tonic phase) and jerking (clonic phase), loss of consciousness, and postictal confusion. - **Absence Seizures:** Brief staring spells, usually without a loss of muscle tone. EEG shows a spike-wave pattern. 2. **Focal Onset Seizures:** Originate in a specific brain region. - **Focal Aware Seizures:** No loss of consciousness; involve motor, sensory, or autonomic symptoms. - **Focal Impaired Awareness Seizures:** Loss of consciousness or altered awareness; may involve repetitive movements or emotional changes. 3. **Psychogenic Nonepileptic Seizures (PNES):** Resemble seizures but are related to psychological factors. Diagnosis often requires video-EEG monitoring. **Complications** - **Status Epilepticus (SE):** A neurological emergency with continuous or rapidly recurring seizures. Requires immediate medical intervention to prevent severe complications like brain damage. - **Physical Risks:** Injury from falls, drowning, or burns. - **Psychosocial Impact:** Stigma, depression, and anxiety are common. Seizure disorders can affect employment, education, and personal relationships. **Diagnostic Studies** - **EEG:** Essential for diagnosing seizures but may not always show abnormalities. Continuous or video-EEG monitoring may be necessary. - **Imaging:** CT, MRI, and other imaging techniques can identify structural abnormalities. - **Blood Tests:** Rule out metabolic or systemic causes. **Interprofessional Care** Seizures generally do not require emergency care unless they are severe or new. For generalized tonic--clonic seizures, emergency care may be necessary. **Medication Therapy** is the mainstay of treatment: - **Anticonvulsants:** Aim to stabilize nerve cell membranes and prevent seizures. Examples include: - **Phenytoin (Dilantin):** Used for tonic--clonic and focal seizures. Administer IV slowly to avoid hypotension. - **Carbamazepine (Tegretol):** Effective for focal seizures. Avoid grapefruit juice and be cautious of abrupt withdrawal. - **Divalproex (Epival ECT):** Used for various types including generalized onset nonmotor and myoclonic seizures. - **Ethosuximide (Zarontin):** Specifically for absence seizures. **Treatment Adjustments:** - **Therapeutic Range Monitoring:** Ensures efficacy and prevents toxicity. - **Combination Therapy:** May be necessary if a single medication is insufficient **Medication Therapy** Anticonvulsant medications are the cornerstone of treatment for seizure disorders, aiming to stabilize nerve cell membranes and prevent the spread of epileptic discharges. Here's a closer look at key aspects: **1. Serum Albumin and Phenytoin Monitoring:** - **Serum Albumin Levels:** These should be monitored alongside serum phenytoin levels, as phenytoin is highly protein-bound. Alterations in serum albumin can affect the free (active) levels of phenytoin. - **Phenytoin (Dilantin) Monitoring:** It's crucial to measure phenytoin serum levels regularly to ensure they remain within the therapeutic range. Abrupt discontinuation can lead to seizures or worsening of the condition. **2. Adverse Effects:** - **CNS Effects:** Common adverse effects include diplopia, drowsiness, ataxia, and cognitive slowing. Regular neurological assessments are necessary to detect dose-related toxicity. - **Non-CNS Effects:** These include skin rashes, gingival hyperplasia, blood dyscrasias, liver, and kidney dysfunction. Regular monitoring and patient education on these risks are vital. For instance, gingival hyperplasia, a common issue with phenytoin, can often be managed with good dental hygiene or surgical intervention if necessary. - **Medication Alert:** Phenytoin should be discontinued at the first sign of a rash, and alcohol intake should be monitored as it can affect serum levels. **3. Nonadherence Issues:** - Patients may struggle with adherence due to adverse effects or the complexity of the medication regimen. Strategies to enhance adherence should be discussed with the patient, potentially involving adjustments to their medication regimen. **Surgical Therapy** Surgical options may be considered for patients whose epilepsy is resistant to medication. **1. Indications for Surgery:** - Candidates typically have a well-defined epileptogenic zone, have not achieved satisfactory seizure control with medications, and have a clear electroclinical syndrome. **2. Success Rates:** - Approximately 30% of epilepsy patients are candidates for surgery, and about 80% are seizure-free five years post-surgery, with 72% maintaining freedom from seizures at ten years. **3. Preoperative Evaluation:** - Involves extensive testing including continuous EEG monitoring to precisely locate the seizure focus. **Alternative Therapies** For patients who do not respond to medication or surgery, several alternative therapies can be considered: **1. Vagal Nerve Stimulation (VNS):** - **Mechanism:** Involves an implanted electrode in the neck that delivers electrical impulses to the vagus nerve. - **Adverse Effects:** Includes coughing, hoarseness, dyspnea, and neck tingling. The device's battery typically lasts 5 to 10 years. **2. Responsive Neurostimulation (RNS):** - **Mechanism:** Similar to a pacemaker, it monitors EEG activity and delivers electrical stimulation to specific brain areas. - **Usage:** Suitable for patients who are not surgical candidates or have multiple seizure foci. **3. Ketogenic Diet:** - **Mechanism:** A high-fat, low-carbohydrate diet that induces ketosis, potentially reducing seizure frequency. - **Considerations:** Requires careful dietary planning and monitoring, particularly if the patient is on vitamin K antagonists like warfarin. **4. Biofeedback:** - **Mechanism:** Uses sensors to monitor brain waves and teach patients to maintain frequencies resistant to seizure activity. - **Effectiveness:** Studies show it can reduce seizure frequency in over 70% of patients with medication-resistant epilepsy. **Health Promotion** 1. **Prevention of Complications:** - **Head Injury Prevention: Encourage the use of helmets to reduce the risk of head injuries during seizures, especially for patients with frequent or uncontrolled seizures.** - **Perinatal Care: Advocate for optimal prenatal and perinatal care to minimize fetal trauma and hypoxia, which can reduce the risk of developing seizure disorders later in life.** 2. **General Health Maintenance:** - **Diet and Rest: Promote a balanced diet, sufficient rest, and regular exercise as part of overall health management.** - **Identifying Triggers: Assist patients in identifying and managing seizure triggers, such as stress, excessive alcohol intake, fatigue, and lack of sleep.** - **Stress Management: Educate patients on stress reduction techniques and the importance of maintaining a routine to minimize the risk of seizure episodes.** **Acute Intervention** 1. **Seizure Observation and Documentation:** - **Detailed Recording: During a seizure, meticulously record:** - **Preceding Events: Any activities or conditions that occurred before the seizure.** - **Timing: Exact time of onset and duration of each phase of the seizure.** - **Nature of the Seizure: Characteristics of the seizure such as loss of consciousness, tongue biting, automatisms, muscle stiffening, jerking, and loss of muscle tone.** - **Body Involvement: The body parts involved and the sequence of involvement.** - **Autonomic Signs: Any signs like dilated pupils, excessive salivation, altered breathing, cyanosis, flushing, diaphoresis, or incontinence.** - **Postictal Assessment: Document the patient's condition after the seizure, including:** - **Level of Consciousness: Awareness and responsiveness.** - **Vital Signs: Blood pressure, heart rate, respiratory rate.** - **Memory and Speech: Any memory loss, speech disorders (e.g., aphasia, dysarthria).** - **Muscle Soreness or Weakness: Any muscle soreness or paralysis.** - **Sleep: Duration and quality of postictal sleep.** 2. **Safety Measures During a Seizure:** - **Airway Management: Maintain a patent airway by turning the patient to the side to prevent tongue occlusion.** - **Head Protection: Protect the patient's head by placing a soft cushion or padding if possible. If seated, ease the patient to the floor gently.** - **Avoid Restraints: Do not attempt to restrain the patient or hold them down.** - **Avoid Objects in Mouth: Do not place any objects in the patient's mouth, as this can cause injury.** 3. **Post-Seizure Care:** - **Repositioning: Assist with repositioning the patient as needed.** - **Suctioning and Oxygen: Ensure that suctioning and oxygen equipment are available and functioning properly for patients with a history of seizures.** - **Education and Reassurance: Provide information to the patient and any witnesses about the seizure. Address any misconceptions and explain the nature of the seizure and its management.** **Psychosocial Interventions** 1. **Emotional Support:** - **Addressing Fear and Anxiety: Seizures can be distressing for both the patient and observers. Provide reassurance and support to help alleviate fear and anxiety.** - **Understanding and Education: Use the opportunity to educate the patient and their family about the seizure disorder, including triggers, treatment options, and what to expect.** 2. **Ongoing Support:** - **Regular Follow-Up: Schedule regular follow-up appointments to monitor the patient's condition and adjust treatment as needed.** - **Support Resources: Connect patients and families with support groups and resources to help manage the emotional and social impacts of living with a seizure disorder.** **Canadian Clinical Skills: Essentials Collection** - Assessing the Neurologic System: Mental Status and Cranial Nerves - Assessing the Neurologic System**:** Motor and Sensory Systems