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Neurologic Disorders
1. Neurotrauma
Head Injuries Head injury is a broad classification that includes injury to the scalp, skull, or brain. It is the most common cause of death from trauma. Traumatic brain injury is the most serious form of head injury. -There are three major components of head injury:- Scalp injury Skull fracture, and Brain injury Skull Fracture One of the most serious types of direct head injury is skull fracture Simple linear skull fracture:- break in continuity of the bone. Depressed skull fracture: When bone fragments are imbedded into brain tissues. Basilar skull fracture: -fracture of base of the skull and may be associated with: - Leakage of CSF from nose (rhino rhea)
- Leakage of CSF from ear (Otto rhea)
- Laceration of vessels of durra leads to intracranial bleeding. Brain Injuries Injury to the brain parenchyma:- Closed (blunt) brain injury occurs when the head accelerates and then rapidly decelerates or collides with another object and brain tissue is damaged, but there is no opening through the skull and dura. Open brain injury occurs when an object penetrates the skull, enters the brain, and damages the soft brain tissue in its path (penetrating injury), or when blunt trauma to the head is so severe that it opens the scalp, skull, and dura to expose the brain.
Pathophysiology Damage to the brain from traumatic injury takes two forms:
- Primary Head injury
- Secondary Head injury a) Primary Head Injury : - Primary injury is the initial damage to the brain that results from the traumatic event. Primary head injury in which damage is due to the impact. Includes Concussion and contusions. Concussion : - Momentary interruptions of brain function with or without loss of consciousness. A cerebral concussion after head injury is a temporary loss of neurologic function with no apparent structural damage. Recover within 24 hours. Headache, irritability, insomnia, poor concentration could persist for months. (Post concussion syndrome) Giving the patient information, explanations, and encouragement may reduce some of the problems of postconcussion syndrome. Observe for the following signs and symptoms:
- Difficulty in awakening
- Difficulty in speaking
- Confusion
- Severe headache
- Vomiting
- Weakness of one side of the body Contusion: - In severe head injury; there is cerebral contusion, tearing and shearing of brain structures which may lead to neurological deficits like hemiplegia. Injuries to the blood vessels cause accumulations of blood in the cranial cavity. N.B:- Since brain floats freely in the CSF, bouncing of brain in this closed confined rigid skull results in concussion or contusion called Coup and counter coup injury. Coup: - injury on the side of impact (below site of impact).
- An abnormal variation in intracranial volume with subsequent change in ICP can be caused by a volume change in any of the three intracranial components. Example : An increase in tissue volume results from brain tumors, brain edema, or bleeding into brain tissue. An increase in blood volume develops when there is vasodilatation of cerebral vessels or obstruction of venous out flow. Excess production, decreased absorption, or obstructed circulation of CSF affords the potential for an increase in CSF component. Brain tumors change in volume occurs slowly. But from head injury change in volume develops rapidly. Compensatory Mechanisms for Increased ICP:- CSF and blood volumes: – are capable of compensating increased ICP. CSF production is constant but reabsorption can vary for adjustment (by pressure difference between CSF in subarachnoid space and blood in dural sinuses). Because changes in ICP produce an increase in CSF pressure without increasing dural sinus pressure reabsorption of CSF will increase. The impact of increase in blood, brain tissue or CSF volume on ICP varies among individuals and depends on the amount of increase that occurs, the effectiveness of compensation mechanisms and cerebral elasticity and plasticity.
- Blood vessels: - elastic component.
- Brain tissue: - plastic component.
- CSF: - Reabsorption. When the CSF and blood can no longer compensate for increased volume and the excess space in the cranial cavity is filled, the ICP rises sharply and may result in cerebral hypoxia or brain shift. When the pressure in the cranial cavity approaches or exceeds the mean systemic arterial pressure, tissue perfusion becomes inadequate, cellular hypoxia results and if maintained, neuronal death may occur. The highly specialized cortical neurons are the most sensitive to 0xygen deficits decreased in level of conciseness is one of the earliest and most reliable sign of Increased ICP.
The increased cellular hypoxia leads to general neurological deterioration. The level of consciousness may deteriorate from alertness through confusion, lethargy, obtundation, stupor, and coma. One of the late reflexes seen with marked increased in ICP is CNS ischemic response; which is triggered by ischemia of vasomotor centre in brain stem. Neurons in vasomotor centre respond directly to ischemia by producing a marked increase in mean arterial blood pressure. Sometimes up to 270mmHg is accompanied by widening of pulse pressure and a reflex slowing of the heart rate. These triads of signs sometimes called the Cushing reflex is important but late indicator of increased ICP. Manifestations of Increased ICP Indirectly the following clinical features can serve as physiologic parameters to asses raised ICP:-
- Cushing Reflex: - Raised Blood Pressure, -Slow Pulse Rate, -Widening of pulse pressure.
- Pupillary response alteration, and
- Change in level of consciousness that change with increase in ICP.
- Projectile vomiting.
- Severe global head ache. 3. HYDROCEPHALUS One form of increased volume in the cranial cavity is hydrocephalus, which is defined as an abnormal increase in CSF volume within any part or all of the ventricular system. Causes: - Decreased absorption of CSF : - -Decreased absorption of CSF can be caused by two Mechanisms: -
- Block in CSF path way to arachnoids villi (None communicating hydrocephalus) Common causes are:- -Congenital malformations Pathophysiology There are two types of brain edema:- a) Vasogenic Brain Edema:- Increased extra cellular fluid that surrounds brain cells. Occurs in conditions like: - Brain tumors.
5. Cerebrovascular disease Ischemic Stroke An ischemic stroke, cerebrovascular accident (CVA), is a sudden loss of function resulting from disruption of the blood supply to a part of the brain. This event is usually the result of long-standing cerebrovascular disease. Only 8% of ischemic strokes result in death within 30 days. Ischemic strokes are subdivided into five different types according to their cause: Large artery thrombosis (20%), Small penetrating artery thrombosis (25%), Cardiogenic embolic stroke (20%), Cryptogenic (30%) and Other (5%). Large artery thrombotic strokes are due to atherosclerotic plaques in the large blood vessels of the brain. Thrombus formation and occlusion at the site of the atherosclerosis result in ischemia and infarction. Small penetrating artery thrombotic strokes affect one or more vessels and are the most common type of ischemic stroke. Small artery thrombotic strokes (lacunar strokes) because of the cavity that is created once the infarcted brain tissue disintegrates. Cardiogenic embolic strokes are associated with cardiac dysrhythmias, usually atrial fibrillation. Emboli originate from the heart and circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. Embolic strokes may be prevented by the use of anticoagulation therapy in patients with atrial fibrillation. The last two classifications of ischemic strokes are cryptogenic strokes, which have no known cause, and other strokes, from causes such as cocaine use, coagulopathies, migraine, and spontaneous dissection of the carotid or vertebral arteries. Pathophysiology
In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of a blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic events referred to as the ischemic cascade
Class D- an "incomplete" - spinal cord injury where motor function is preserved below the neurological level and more than half of the key muscles below the neurological level have a muscle grade of more than 3. Over 95% of people with "incomplete" spinal cord injury recover locomotory ability. Class E - normal- where motor and sensory functions are normal. The is 100% recovery. Pathophysiology and Etiology SCI may result from trauma, vascular disorders, infectious conditions, tumor SCI can affect upper motor neurons (UMN) or lower motor neurons (LMN).
- UMNs extend from the motor strip in the cerebral cortex of the brain through the corticospinal tract in the spinal cord, where they synapse with interneurons in the ventral horn.
- UMN lesions at T 12 and above result in spasticity.
- LMNs originate in the ventral horn , exit the spinal cord at each segment, and extend to the neuromuscular junction.
- Each LMN innervates 10 to 2,000 muscle fibers.
- LMN lesions at L 1 and below result in flaccidity and reflex loss. Clinical Manifestations Patients with tetraplegia (formerly called quadriplegia) have damage to the cervical segments of nerves (C1-C8) in the spinal canal. Function may be impaired in the upper extremities, trunk, pelvic organs, and lower extremities. Patients with paraplegia (hemiplegia) have damage to the thoracic, lumbar, or sacral segments of nerves in the spinal cord. The arms are unaffected, but function may be impaired in the trunk, pelvic organs, and lower extremities. The following grading is suggested: 0 = Total paralysis 1 = Contraction visible or palpable 2 = Active movements and full ROM without gravity
3 = Active movement and full ROM against gravity 4 = Active movement and full ROM with moderate resistance 5 = Normal motor with active movement and full ROM against full resistance Diagnostic Evaluation X-ray of spinal column MRI of spine.--to detect soft tissue injury, hemorrhage, edema, bony injury;
6. Seizure disorders,
Seizures are episodes of abnormal motor, sensory, autonomic, or psychic activity resulting from sudden excessive discharge from cerebral neurons. A part or all of the brain may be involved. The international classification of seizures differentiates between two main types: Partial seizures that begin in one part of the brain, and Generalized seizures that involve electrical discharges in the whole brain. Most seizures are sudden and transient. The underlying cause is an electrical disturbance in the nerve cells in one section of the brain, causing them to emit abnormal, recurring, uncontrolled electrical discharges. There may be associated: Loss of consciousness, Excess movement or loss of muscle tone or movement, and Disturbances of behavior, mood, sensation, and perception. The specific causes of seizures are varied and can be categorized as
- Idiopathic (genetic, developmental defects) and
- Acquired: caused by hypoxemia of any origin, including vascular insufficiency, fever (childhood), head injury, hypertension, central nervous system infections,
Complex partial seizures (with complex symptoms, generally with impairment of consciousness)
- With impairment of consciousness only
- With cognitive symptoms
- With affective symptoms
- With psychosensory symptoms
- With psychomotor symptoms (automatisms)
- Compound forms **Types of seizures
- Partial seizures –** produced by a small part of brain - Simple : simple motor, simple sensory, simple psychological - Complex: impairment of awareness- automatism - Partial seizure with secondary generalization 2. Generalized Seizures (convulsive or nonconvulsive, bilaterally symmetric, without local onset) i. Grand mal/ Tonic seizures ii. Tonic-clonic seizures iii. Clonic seizures iv. Absence seizures v. Atonic seizures vi. Myoclonic seizures (bilaterally massive epileptic)
1. STATUS EPILEPTICUS
Status epilepticus (acute prolonged seizure activity) is a series of generalized seizures that occur without full recovery of consciousness between attacks. It is considered a medical emergency. Status epilepticus produces cumulative effects. Vigorous muscular contractions impose a heavy metabolic demand and can interfere with respiratory and cardiac functions.
There is some respiratory arrest at the height of each seizure that produces venous congestion and hypoxia of the brain. Repeated episodes of cerebral anoxia and edema may lead to irreversible and fatal brain damage. Factors that precipitate status epilepticus include withdrawal of antiseizure medication, fever, and concurrent infection. Pathophysiology and Etiology Altered Physiology The pathophysiology of seizures is unknown. It is known, however, that the brain has certain metabolic needs for oxygen and glucose. Neurons also have certain permeability gradients and voltage gradients that are affected by changes in the chemical and humoral environment. Factors that change the permeability of the cell population (ischemia, hemorrhage) and ion concentration (Na+, K+) can produce neurons that are hyperexcitable and demonstrate hypersynchrony, producing an abnormal discharge. A seizure may manifest itself as an alterred behavior, motor, or sensory function relating to any anatomical location in the brain. Classification Seizures are classified by the origin of the seizure activity and associated Clinical Manifestations Manifestations are related to the area of the brain involved in the seizure activity and may range from single abnormal sensations, aberrant motor activity, altered consciousness or personality to loss of consciousness and convulsive movements. Impaired consciousness Disturbed muscle tone or movement Disturbances of behavior, mood, sensation, or perception Disturbances of autonomic functions Simple partial seizures can have motor, somatosensory, psychic, or autonomic symptoms without impairment of consciousness. Complex partial seizures have an impairment (but not a loss) of consciousness with simple partial features, automatisms, or impairment of consciousness only.
The size of both pupils. Are the eyes open? Did the eyes or head turn to one side?
- The presence or absence of automatisms (involuntary motor activity, such as lip smacking or repeated swallowing)
- Incontinence of urine or stool
- Duration of each phase of the seizure
- Unconsciousness, if present, and its duration
- Any obvious paralysis or weakness of arms or legs after the seizure
- Inability to speak after the seizure
- Movements at the end of the seizure
- Whether or not the patient sleeps afterward
- Cognitive status (confused or not confused) after the seizure
7. Intra cranial infection Intra cranial infection is one of a common and fatal condition. It may occur following head injury or spontaneously. The infectious disorders of the nervous system include meningitis, brain abscesses , various types of encephalitis Meningitis:- Meningitis is an inflammation of the meninges, of the brain and spinal cord Inflammation of pia mater , subarachnoids mater & space. Caused by infection, but chemicals could cause. Meningitis is classified as aseptic or septic. In aseptic meningitis, is caused by the viral , lymphoma , leukemia, or brain abscess. Septic meningitis is caused by bacteria, like Neisseria meningitidis , Haemophilus influenzae and Streptococcus pneumoniae. NB: Outbreaks of N. meningitidis infection are most likely to occur in dense community groups, such as college campuses and military installations. Factors that increase the risk for developing bacterial meningitis include Tobacco use and viral upper respiratory infection because they increase the amount of droplet production. Otitis media and mastoiditis increase the risk of bacterial meningitis because the bacteria can cross the epithelium membrane and enter the subarachnoid space. Persons with immune system deficiencies Pathophysiology N. meningitidis concentrates in the nasopharynx and is transmitted by secretion or aerosol contamination. Meningococcal meningitis occurs as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS). Once the causative organism enters the bloodstream, it crosses the blood-brain barrier and causes an inflammatory reaction in the meninges.
- Neurosurgery
- Systemic sepsis,
- Immune compromised host. Most common symptoms and signs: - Fever, chills: - due to release of inflammatory mediators and endotoxins. Headache: - due to increased ICP as the result of inflamed Meninges. Photophobia: - due to raised ICP Nausea & vomiting: - due to raised ICP Neck pain & neck stiffness Positive Meningeal signs:- Kernig's sign -resistance to extension of leg while the patient is lying with the hip flexed at right angle. Brudzinski sign: when forcible flexion of the neck results in flexion of hip and knee. N.B - The path physiologic mechanisms of these signs are due to stretching of inflammed meninges, which results in pain upon performing the maneuvers.
Encephalitis
Encephalitis is inflammation of the brain. There are several causes, but the most common is viral infection. Encephalitis often causes only mild flu-like signs and symptoms — such as a fever or headache — or no symptoms at all. Sometimes the flu-like symptoms are more severe. Encephalitis can also cause confused thinking, seizures, or problems with senses or movement. Rarely, encephalitis can be life-threatening. Timely diagnosis and treatment are important because it's difficult to predict how encephalitis will affect each individual. Symptoms Children: Bulging fontanel Most people with viral encephalitis have mild flu-like symptoms, such as: Headache Fever Aches in muscles or joints Fatigue or weakness
Sometimes the signs and symptoms are more severe, and might include: Confusion, agitation or hallucinations Seizures Loss of sensation or paralysis in certain areas of the face or body Muscle weakness Problems with speech or hearing Loss of consciousness In infants and young children, signs and symptoms might also include: Bulging in the soft spots (fontanels) of an infant's skull Nausea and vomiting Body stiffness Poor feeding or not waking for a feeding Irritability Causes The exact cause of encephalitis is often unknown. But when a cause is known, the most common is a viral infection. Bacterial infections and noninfectious inflammatory conditions also can cause encephalitis. There are two main types of encephalitis: Primary encephalitis. This condition occurs when a virus or other agent directly infects the brain. The infection may be concentrated in one area or widespread. A primary infection may be a reactivation of a virus that had been inactive after a previous illness. Secondary encephalitis. This condition results from a faulty immune system reaction to an infection elsewhere in the body. Instead of attacking only the cells causing the infection, the immune system also mistakenly attacks healthy cells in the brain. Also known as post- infection encephalitis, secondary encephalitis often occurs two to three weeks after the initial infection. Common viral causes The viruses that can cause encephalitis include: Herpes simplex virus (HSV). Both HSV type 1 — associated with cold sores and fever blisters around your mouth — and HSV type 2 — associated with genital herpes — can cause encephalitis. Encephalitis caused by HSV type 1 is rare but can result in significant brain damage or death. Other herpes viruses. These include the Epstein-Barr virus, which commonly causes infectious mononucleosis, and the varicella-zoster virus, which commonly causes chickenpox and shingles.
