Patho Neurological Disorders PDF

NEUROLOGICAL DISORDER ANATOMY OF THE BRAIN The brain is protected by the skull, cerebrospinal fluid, and three membranes called the meninges. The dura mater is the outermost layer protecting the brain. o It is tough, fibrous, and leather-like tissue. The arachnoid mater is...

NEUROLOGICAL DISORDER ANATOMY OF THE BRAIN The brain is protected by the skull, cerebrospinal fluid, and three membranes called the meninges. The dura mater is the outermost layer protecting the brain. o It is tough, fibrous, and leather-like tissue. The arachnoid mater is the middle protective layer. o It is a thin, delicate, fibrous membrane. The pia mater is the innermost protective layer of connective tissue. TRAUMATIC BRAIN INJURY Traumatic brain injury (TBI) is a disruption of the normal function of the brain caused by an external force. It is the most common cause of death and disability among Canadians 40 years and younger. There are two types of TBI: primary and secondary. Primary TBI is caused by direct impact to the brain. o The injury may be focal, affecting one area, or diffuse, affecting multiple areas. Secondary TBI occurs due to the primary injury. o Examples include cerebral swelling, inflammation, and increased intracranial pressure. Focal Brain Injury Focal brain injuries can result from closed (blunt) or open (penetrating) trauma.  Closed trauma, where the dura remains intact, is the most common type. o Closed trauma can cause focal brain injuries and diffuse axonal injury. A coup injury refers to the brain injury at the site of direct impact of the brain on the skull. A contrecoup injury happens when the brain rebounds and hits the opposite side of the skull. o This results in a secondary area of damage on the opposite side of the brain from the coup injury. When the skull impacts the brain, it can cause a contusion, or bruising within the brain. This "bruising" results from blood leaking from injured vessels. Edema may form, which can lead to increased intracranial pressure. Possible symptoms of a contusion include: Immediate loss of consciousness after trauma for 5 minutes or less. Loss of reflexes Brief loss of respirations Brief episode of bradycardia Hypotension lasting seconds to a few minutes Open Brain Injury Open brain injury occurs when trauma penetrates the dura, such as with crush or stretch injuries. Hematomas Hematomas are collections of blood that form within the skull due to TBI. There are several types: Epidural hematoma: Blood collects between the skull and the dura mater. o Most epidural hematomas are caused by arterial bleeding and are considered an emergency.  They form rapidly.  Typically, a person with an epidural hematoma becomes unconscious, has a moment of lucidity, and then experiences a decreased level of consciousness.  Rapid surgical intervention is necessary. o Venous epidural hematomas are less common and develop slowly. Subdural hematoma: Blood collects between the arachnoid mater and the pia mater.  o It is usually caused by injury to the brain and its blood vessels. o Bleeding is typically venous. o It can be acute, subacute, or chronic.  Acute subdural hematomas occur within 48 hours of injury, and surgery is typically needed to evacuate the hematoma.  Subacute subdural hematomas occur within 2-14 days of injury.  Chronic subdural hematomas can occur weeks to months after an injury. o Symptoms include decreased level of consciousness, confusion, and lethargy. Intracerebral hemorrhage: Bleeding occurs within the brain tissue itself. o It is associated with contusions. o Occurs in 2-3% of persons with head injuries. o Intracerebral hemorrhage can lead to increased intracranial pressure and cerebral edema. o The presence of an intracerebral hematoma may be delayed, presenting 3-10 days after the initial head injury. Diffuse Axonal Injury (DAI) DAI is a severe brain injury characterized by widespread axonal injury, which involves shearing, tearing, or stretching of the nerve fibers. It can occur with mild, moderate, or severe brain injury. It develops 12-24 hours post-brain injury. Signs include decreased level of consciousness, increased intracranial pressure, and cerebral edema. There are several categories of DAI: Mild Concussion o Mild but immediate clinical manifestations o CSF pressure rises o ECG/EEG changes o Glasgow Coma Scale (GCS) score of 13-15 o Confusion lasts 1 to several minutes with amnesia o Headache and nervousness for a few days Classic Cerebral Concussion o Loss of consciousness (LOC) less than 6 hours with amnesia o Confusion o Transient cessation of respiration o Vital signs stabilize within a few minutes DAI (mild, moderate, severe) o Severe brain injury coma lasting more than 6 hours Complications of TBI TBI can lead to several complications, including increased intracranial pressure and cerebral edema. The sources you provided also discuss cerebrovascular disorders, which are a leading cause of disability and the third leading cause of death in Canada, but do not explicitly state whether they are a complication of TBI. You may wish to clarify whether you are interested in learning about these disorders in relation to TBI. CEREBRALVASCULAR DISORDERS: STROKE Ischemic: caused by a blockage of blood flow to the brain. o Thrombotic stroke: Arterial occlusions caused by thrombi formed in arteries supplying the brain or in the intracranial vessels. o Embolic stroke: Fragments that break from a thrombus formed outside the brain and block an artery in the brain. o Lacunar strokes: Occlusion of a single, deep perforating artery causing ischemic lesions in the brain. These strokes are rare. Hemorrhagic: caused by bleeding in the brain. o Hypertension is the primary cause of hemorrhagic stroke. o Bleeding compresses brain tissue, leading to ischemia, edema, increased intracranial pressure (ICP), and necrosis. o Hemorrhagic strokes can be classified by size and shape, including massive, small, slit, and petechial. Hemodynamic or Hypoperfusion: associated with systemic hypoperfusion resulting in inadequate blood supply to the brain. Transient Ischemic Attacks (TIAs) TIAs are a type of ischemic cerebrovascular disorder. They involve neurological dysfunction that lasts less than one hour and results from an ischemic event. TIAs can be a warning sign for a future stroke, as they may predispose a person to a stroke within 90 days. It is important to note that the sources primarily focus on traumatic brain injury and increased intracranial pressure. While they introduce cerebrovascular disorders, they don't provide extensive details about their specific causes, symptoms, or treatments beyond the classifications listed above. Increased Intracranial Pressure (ICP) The intracranial space houses three key components: brain tissue, blood, and cerebrospinal fluid (CSF). CSF is a clear fluid that circulates in the subarachnoid space and ventricles of the brain, providing protection to the brain and spinal cord. Normally, these components exist in a state of equilibrium, maintaining a stable intracranial pressure within a range of 1-15 mm Hg. However, any alteration in the volume of these components disrupts this balance, leading to increased ICP. Causes of Increased ICP Various conditions can contribute to increased ICP by affecting the volume of one or more of the intracranial components: Increased Brain Tissue Volume: Cerebral neoplasms, contusions, abscesses, and cerebral edema can all increase the volume of brain tissue, leading to increased ICP. Increased Blood Volume: Intracranial hematomas, hemorrhages, metabolic and physiological factors, and vascular anomalies can elevate blood volume within the skull, contributing to increased ICP. Increased CSF Volume: CSF-secreting tumors and hydrocephalus can increase the volume of CSF, leading to elevated ICP. Factors such as blood pressure, cardiac function, intra-abdominal and intra-thoracic pressure, body position, temperature, and blood gases, particularly CO2, can also influence ICP. The Monroe Kellie Doctrine The Monroe Kellie Doctrine explains the delicate interplay between the intracranial components and ICP. It states that because the skull is a rigid structure, any increase in the volume of one component must be offset by a decrease in another to maintain a stable ICP. If this compensation fails, ICP will rise. Compensatory Mechanisms The body employs several mechanisms to prevent increased ICP: CSF Volume Compensation: CSF can shift within the cranium, being displaced into the spinal subarachnoid space. Additionally, the production and absorption of CSF can be adjusted. Blood Volume Compensation: Cerebral blood vessels can constrict or dilate to modify blood volume. Venous outflow can also be reduced to compensate for increased brain tissue or CSF volume. Brain Tissue Compensation: Brain tissue has a limited ability to shift within the skull. These mechanisms can maintain normal ICP initially, but they have limitations. When these limits are exceeded, ICP increases. Cerebral Blood Flow and Autoregulation The brain relies on a constant supply of oxygen and glucose, which it cannot store. Autoregulation is the brain's ability to adjust its blood flow according to its metabolic needs. Cerebral blood vessels change diameter to maintain consistent blood flow even with blood pressure fluctuations. This process ensures adequate cerebral perfusion pressure. Several factors influence autoregulation:  PaCO2: An increase in the partial pressure of arterial carbon dioxide (PaCO2) relaxes smooth muscle, decreases cerebrovascular resistance, and increases cerebral blood flow. A decrease in PaCO2 has the opposite effect, reducing cerebral blood flow. PaO2: A decrease in the partial pressure of arterial oxygen (PaO2) below 50 mm Hg causes cerebral vasodilation, decreasing resistance and increasing blood flow. Prolonged low PaO2 leads to anaerobic metabolism, lactic acid accumulation, and acidosis, ultimately impairing compensation and potentially causing cell death. Cerebral Perfusion Pressure (CPP) CPP is the pressure required to ensure sufficient blood flow to the brain. Normal CPP ranges from 70 to 90 mm Hg. A decrease in CPP can lead to autoregulation failure, reduced cerebral blood flow, ischemia, and cell death. Conversely, excessively high mean arterial pressure (MAP) can increase CPP, potentially causing or worsening cerebral edema. Cerebral Edema Cerebral edema, an increase in brain tissue fluid content, often results from TBI but can also be caused by infection, hemorrhage, tumor, ischemia, infarction, and hypoxia. It contributes to increased ICP as fluid accumulates in the brain's extravascular spaces. There are three types of cerebral edema: Vasogenic: The most common type, characterized by increased permeability of capillary endothelium due to injury. This allows plasma proteins to leak into the extracellular space, drawing water and increasing fluid content. Vasogenic edema originates at the injury site and spreads, causing focal neurological deficits, decreased level of consciousness, and severe ICP elevation. Cytotoxic: Occurs due to cell membrane disruption caused by trauma or lesions that lead to oxygen deprivation and loss of cellular transport systems. Fluid and proteins shift from the extracellular to the intracellular space, causing cell swelling and potential death. The earliest symptom is a decreased level of consciousness. Interstitial: Primarily observed in hydrocephalus, involving fluid accumulation in the brain's interstitial spaces. Patients may experience more than one type of cerebral edema simultaneously. Clinical Manifestations of Increased ICP Increased ICP can manifest in various ways, including: Pupillary Changes: Compression of the oculomotor nerve (CN III) can cause sluggish pupillary reaction to light, dilation, or inability to move. A fixed, dilated, and unresponsive pupil is an emergency, indicating brain herniation. Vision Changes: Blurred vision, double vision (diplopia), and altered extraocular eye movements can occur.  Motor Function Impairment: Hemiparesis (weakness on one side of the body), hemiplegia (paralysis on one side of the body), and abnormal posturing such as decorticate or decerebrate posturing can develop. Headache: Pain may result from compression of intracranial structures. Vomiting: Often projectile and without nausea. Diagnosis and Management of Increased ICP Diagnosing the underlying cause of increased ICP is crucial. Diagnostic tools include CT scans, MRIs, and ICP monitoring in intensive care units. Management strategies aim to reduce ICP and address the underlying cause: ICP Monitoring: Allows for continuous assessment of ICP levels. Surgical Intervention: May be necessary to remove masses, evacuate hematomas, or relieve pressure. Mannitol: An osmotic diuretic administered intravenously to reduce ICP by drawing water from the brain tissue.  Corticosteroids: Used to decrease vasogenic edema caused by tumors or abscesses, but not routinely used in head injuries. Mechanical Ventilation: May be required to maintain adequate oxygenation and ventilation. Nutritional Therapy: Early initiation of nutrition within five days of TBI has been shown to improve outcomes. Tube feeding or total parenteral nutrition (TPN) can be used. Brain Herniation: A Life-Threatening Complication Brain herniation occurs when increased ICP forces brain tissue to shift from its normal position, potentially compressing vital structures like the brainstem. Herniation affecting the cerebellum and brainstem can lead to respiratory arrest and death if not promptly treated. Treatment for brain herniation is an emergency and may include: CSF Drainage Steroid Administration to Reduce Swelling Mannitol Administration Intubation Surgery to Remove Part of the Skull or Brain Tissue The provided sources include case studies that illustrate various aspects of increased ICP and its management. You can use these case studies to test your understanding and further explore the complexities of this condition.