MSP Unit 3

Overview

• The nervous system consists of the central nervous system(brain & spinal cord) and the peripheral nervous system.
• The central nervous system (CNS) controls and regulates all mental and physical functions.
• CNS disease or trauma may damage several types of tissues locally or one type of tissue throughout many areas.

Upper and Lower Motor Neuron Lesions

• Upper Motor Neuron (UMN) lesions feature increased muscle tone, clonus, and spasticity.
• UMN lesions feature increased deep tendon reflexes.
• Lower Motor Neuron (LMN) lesions feature reduced or absent muscle tone.
• LMN lesions feature reduced deep tendon reflexes.
• Flaccid paralysis is a characteristic of lower motor neuron (LMN) lesions.

Aging and the Central Nervous System

• A simple loss of cells is common with aging
• Nerve cell shrinking occurs
• Velocity decreases in the myelinated fibers.
• Loss in blood supply occurs.
• Other aging changes are not well established.

Peripheral Nervous System Changes with Aging

• Fascicles remain unaffected with aging.
• The perineurium and epineurium tend to thicken.
• The endoneurium often becomes fibrosed.
• There are changes to blood vessels supplying nerves
• Sympathetic control of dermal vasculature leads to diminished wound repair efficiency.
• ANS dysfunction is more common in the peripheral nervous system than in the central nervous system due to aging.
• Altered axonal myelination occurs in the peripheral nervous system with aging.
• Loss of fibers and sensory alterations occur in the peripheral nervous system due to aging.
• Peripheral neuropathy occurs in the peripheral nervous system due to aging
• Diffuse weakness is an effect of aging on the peripheral nervous system.

Cranial Nerves Overview

• There are 12 pairs of cranial nerves.
• The cranial nerves are numbered based on the order they arise from the nuclei in the brain
• Cranial nerves XI (accessory) & XII (hypoglossal) are excluded from this numbering rule.
• The cranial nerves are: I-Olfactory, II-Optic, III-Oculomotor, IV-Trochlear, V-Trigeminal, VI-Abducens, VII-Facial, VIII-Vestibulocochlear, IX-Glossopharyngeal, X-Vagus, XI-Accessory, XII-Hypoglossal
• Cranial nerves can be: sensory, motor, or both.

Cranial Nerve Involvement

• Fracture of the cribriform plate can damage the olfactory nerve (CN I), resulting in anosmia and cerebrospinal fluid rhinorrhea.
• Direct trauma to the orbit or optic canal fracture can impact the optic nerve (CN II), causing loss of pupillary constriction.
• Pressure on the optic pathway, or laceration/intracerebral clots in the temporal, parietal, or occipital lobes of the brain can impact the optic nerve (CN II), causing visual field defects.
• Pressure from herniating uncus or fractures involving the cavernous sinus, or aneurysms can damage the Oculomotor nerve (CN III).
• Damage to the Oculomotor nerve causes a dilated pupil, ptosis, eye turning down and out as well as a loss of pupillary reflex.
• Stretching of the trochlear nerve around the brainstem or orbit fractures can impact the trochlear nerve (CN IV)
• Damage to the trochlear nerve results in the inability to look down when the eye is adducted.
• Injury to the terminal branches of the trigeminal nerve (CN V), pathological processes affecting the trigeminal ganglion result in a loss of pain and touch sensations as well as paraesthesia
• With CN V damage, the masseter and temporalis muscles will not contract along with mandible deviation to the lesion side when the mouth is opened
• A base of brain or fracture involving the cavernous sinus or orbit can damage the abducens nerve (CN VI), resulting in the eye not being able to move laterally and diplopia on lateral gaze.
• Laceration or contusion in the parotid region can damage the facial nerve (CN VII), resulting in paralysis of facial muscles meaning the eye remains open, the angle of the mouth droops, and the forehead does not wrinkle.
• Temporal bone fractures can damage the facial nerve (CN VII).
• Intracranial hematomas ("stroke") can affect the facial nerve (CN VII)
• Vestibulocochlear nerve (CN VIII) damage results in progressive unilateral hearing loss and tinnitus.
• Brainstem lesions or deep lacerations of the neck can damage the glossopharyngeal nerve (CN IX), resulting in a loss of taste on the posterior third of the tongue as well as the loss of sensation on the affected side of the soft palate
• Brainstem lesions or deep lacerations of the neck can damage the vagus nerve (CN X), resulting in sagging of the soft palate, uvula deviation to the normal side, and hoarseness from vocal paralysis.
• Lacerations of the neck can affect the spinal accessory nerve (CN XI), resulting in paralysis of the sternocleidomastoid and descending fibers of the trapezius as well as shoulder droop.
• Neck lacerations or fractures of the cranial base can affect the hypoglossal nerve (CN XII), resulting in the protruded tongue deviating toward the affected side and moderate dysarthria.

Peripheral Nerves and Injury

• The nervous system acts as a mechanical, electrical, and chemical continuum.
• Types of stresses that can lead to injury are: Immobilization, Repetitive Friction, Compression and Lengthening/Stretching
• Tension, Compression, and Sliding are all part of the physical stress theory that can lead to stress

Nerve Injury Classifications

• Neuropraxia involves a temporary disruption of nerve function without any structural damage.
• Segmental demyelination occurs with Neuropraxia.
• Conduction of the action potential is normal on both sides with Neuropraxia
• There is no muscle atrophy with Neuropraxia
• Axonotmesis is damage to both the nerve fibers and the surrounding tissue.
• Axonotmesis produces an infarction and necrosis.
• Neurotmesis involves a complete disruption or severing of the nerve fibers and surrounding tissue.
• Wallerian degeneration is an active process of degeneration that results from a cut or crush, and the part of the axon distal to the injury degenerates.
• When axonal continuity is lost (axonotmesis or neurotmesis), axons distal to the lesion degenerate.

Nerve Injuries

• Compression distorts or changes the shape of neural structures based on applied pressures.
• The epineurium provides primary protection against excessive compression and has a spongy quality.
• Venous flow from the nerve is reduced from 30 to 50 mmHg of compression
• Nerve failure occurs over one hour with compression
• Transverse Contraction can lead to nerve injury

Viscoelastic Behavior of Nerves

• Healthy intraneural blood flow is sensitive to oxygen deprivation.
• Nerves have their own nerve innervation, known as Nervi nervorum.
• Nervi nervorum are a source of nociception and pain.
• Neurogenic Inflammation occurs when a sensitized nerve produces inflammation into its innervated tissue.
• Neurogenic inflammation can lead to tissue inflammation, trigger points, and joint degeneration.

Neuropraxia

• Neuropraxia occurs from a reduction in nerve conduction at the site of injury due to compression, traction, and repetitive movements (friction).
• Ischemia and Schwann cell damage cause Neuropraxia
• Functional recovery with Neuropraxia occurs in minutes, weeks, or a couple of months
• Neuropraxia is the least severe injury
• Conduction across the zone of nerve injury is inhibited, but conduction within the nerve both proximal and distal to the lesion remains intact with Neuropraxia
• The continuity of all structures is preserved with Neuropraxia
• Wallerian degeneration does not occur with Neuropraxia (no axonal loss).
• Tissue anoxia, local ischemia, nerve fiber deformation, vascular permeability, intraneural edema, and fibroblastic proliferation are a biological response to injury causing compression, traction & friction Neuropraxia.
• Neurogenic Inflammation is an inflammatory reaction that can contribute to nerve injuries that includes: vasodilation, plasma extravasation and chemotaxis, edema, sensitization of nerve endings
• Neurogenic Inflammation also causes: waking of sleeping or ineffective nociceptors and up-regulation of DRG
• Vasodilation, bradykinin and norepinephrine, and adrenal glands influence sympathetically mediated inflammation.
• Intraneural edema increases following nerve injury.
• Intraneural edema causes a pressure increase.
• Poor edema resolution and mechanical constriction and inflammatory byproducts further decrease blood flow and perpetuates congestion within the nerve

Neurotmesis

• With Neurotmesis, the nerve is severed, resulting in the loss of axon and connective tissue continuity.
• Neurotmesis can result from gunshot wounds, stab wounds, avulsion injuries, stabs, or cuts.
• Neurotmesis depends on the nerve involved and injury factors.
• In peripheral nerve distribution distal to lesion there is flaccid paralysis of muscles with Neurotmesis.
• If left untreated, health declines in target tissue and rapid atrophy occurs with Neurotmesis.
• Loss of sensory and sympathetic function occurs with Neurotmesis
• Surgery is required to address Neurotmesis and primary repair is preferred.
• After coaptation or autograft, repair site protection is the most important factor.
• Postoperative splinting maintains slack in the nerve, and compressive dressings decrease venous congestion and edema with Neurotmesis. Conective Nerve Tissue Conduit Healing for nerve injuries that is used to assist Neurotmesis is broken down into 3 phases:
• Inflammation, lasts up to 3 days with most activity within the first 48 hours
• Repair lasts from day 4 - day 21
• Remodeling/Maturation lasts from 21 days to several months
• After complete axonal transection, the neuron undergoes a degenerative process, Wallerian Degeneration, and pain can be expected
• It takes 2-3 weeks up to 2 years for Remodeling/Maturation to occur after connective tissue repair with an increase in cross links and type 3 to type 1 collagen
• After connective tissue repair, axons regenerate an average of 1 to 2 mm per day and connective tissue can repair in 21 days to several months.
• Recovery depends on the repair length of the nerve and whether it was repaired after neurotmesis
• Muscles atrophy rapidly after transection, irreversibly changing after 2 years to become fibrotic
• There's no hope when reinnervation takes longer or delays function after 1 year with 18-24 months.

Axonotmesis

• APeripheral Nerve Injury, damage or injury to the axons occurs and is called Axonotmesis.
• Epineurium/perineurium/endoneurium remains intact with Axonotmesis.
• Axonotmesis is caused by severe compression, friction/shear, or traction
• Axonotmesis is caused by prolonged low loads or short duration high loads
• Surgery is often required to achieve recovery with Axonotmesis
• Surgical release of transverse carpal ligament in CTS and Decompression of associated anatomical structures are used with Axonotmesis to treat.

Peripheral Nervous System Disorders

• Somatic motor and sensory components of cranial and spinal nerves are a part of the peripheral nervous system (PNS).
• PNS disorders can be divided into neuropathies and myopathies
• Signs and symptoms of PNS involvement relate to the motor and sensory systems and the ANS

Myasthenia Gravis

• Myasthenia Gravis is an autoimmune disorder whose mechanism of action takes place at the site of the neuromuscular junction and motor end plate.
• Action is caused by blocking, altering,or destroying the receptors for acetylcholine at the neuromuscular junction
• Symptoms include weakness, double vision, and difficulties with speech and chewing.
• Myasthenia Gravis can be treated with Pyridostigmine (Mestinon), neostigmine (Prostigmin) due to its indirect-acting acetylcholinesterase Inhibitor
• This drug inhibits acetylcholinesterase, thereby increasing acetylcholine availability at NMJ and can improve muscle strength and reduces fatigue
• Side effects for this medication include diarrhea, abdominal cramps, increased salivation, and muscle cramps
• Glucocorticoids such as Prednisone are also used to treat Myasthenia Gravis
• Effective in improving symptoms with long-term side effects Osteoporosis, hypertension, hyperglycemia, weight gain, and increased risk of infections.

Guillain-Barré Syndrome (GBS)

• Guillain-Barré Syndrome (GBS) causes Rapidly evolving motor paresis and paralysis and sensory deficits with Maximal weakness within 2 to 3 weeks
• Recovery from GBS takes weeks to months
• Common diagnostic testing includes spinal tap, electromyography (EMG), and nerve conduction studies
• Common symptoms of GBS include Progressive muscle weakness, Tingling and numbness, Loss of reflexes and Pain and discomfort.
• Difficulty with coordination and balance and Difficulty breathing and swallowing are also indicative of GBS

Neuropathy

• Neuropathy results from a wide variety of causes with many classifications i.e. number, rate, onset, size
• Initial features of Neuropathy include: tingling, prickling, burning, or parasthesias/dysethesias
• Symptoms include: weakness, decreased tone, muscle tenderness, and/or cramping
• Conditions associated With neuropathy are Compression and entrapment syndromes, Hereditary Neuropathies, Metabolic Neuropathies, Diabetic neuropathy, and Alcoholic neuropathy
• Gabapentin (Neurontin®) and Pregabalin (Lyrica®) are traditional anticonvulsants used for seizures, that also treat neuropathic pain such as Diabetic peripheral neuropathy, Post-herpetic neuralgia, and Phantom pain syndrome
• Pregabalin adverse effects include dizziness, drowsiness, and peripheral edema that is mild and tend to resolve
• Gabapentin is also indicated as muscle relaxant for certain types of spasticity

Polio and Post-Polio Syndrome

• Polio is an infectious viral disease caused by the poliovirus.
• Polio Primarily affects the CNS and is transmitted primarily through contamination or by direct contact.
• Post-Polio Syndrome may develop in some individuals who have previously had polio, usually after a significant period of stability following the initial infection and typically occurs 15 to 40 years after the initial polio infection.

Infections of the Central Nervous System

• Meningitis (most common bacterial or viral) causes Inflammation of meninges of the brain & spinal cord
• Myelitis (viral) causes Inflammation of the spinal cord and Intracranial Hemorrhage.

Multiple Sclerosis (MS)

• Multiple sclerosis (MS) is a CNS, autoimmune, demyelinating disorder and a major cause of disability in young adults.
• MS is named due to the descriptive of the sclerotic plaques disseminated throughout the CNS that are the hallmark of the disease.
• Types of MS: Primary Progressive, Secondary Progressive, Progressive Relapsing, and Relapsing-Remitting
• Primary progressive symptoms include steady progression of symptoms and disability from the onset, with little to no remission
• A steadily worsening disease course from the beginning, along with occasional relapses or flare-ups of symptoms is called Progressive-relapsing.
• Distinct relapses or flare-ups of symptoms followed by periods of is called relapsing-remitting
• As MS progresses, there is a steady worsening over time of their symptoms
• Visual problems, fatigue or increased motor weakness with effort, mental fatigue, and sleepiness are common clinical manifestations.
• Spasticity occurs in 90% of cases of MS and can manifest as Spasm or weakness of facial muscles and or abnormal speech
• Drug therapy slows disease progression - injecting Interferons-Interferon beta-la (Avonex) & Interferon beta-lb (Betaseron) & Fingolimod (Gilenya) to managing severe relapses

Amyotrophic Lateral Sclerosis

• Amyotrophic Lateral Sclerosis is a progressive disease of unknown cause
• Characterized by degeneration and scarring of the motor neurons in the corticospinal tract.
• Presents with Tonic atrophy from mix of UMN and LMN lesions, damage in the corticobulbar tract and weakness of muscles involved in swallowing, chewing, and facial gestures.
• ALS is treated Pharmacologically by Riluzole and potentially muscle relaxants.

Parkinson's Disease (PD)

• Parkinson's Disease is caused by Degeneration of the dopamine producing cells in the basal ganglia.
• While it is Primarily idiopathic, although there may be a genetic link in about 10% of cases
• Parkinson's Disease clinical manifestations include: tremor, rigidity, akinesia or bradykinesia and a slow shuffling gait.
• Parkinsonism clinical manifestations include those of Parkinson's Disease in addition to others.
• Iatrogenic (drug-induced) parkinsonism results from agents that block or interfere with dopamine metabolism.
• Diminished response to Levodopa can lead to progressive loss in effectiveness. Common Drug Therapies for Parkinson's Disease:
  • Levodopa and Carbidopa: converted into dopamine by inhibiting enzyme after it crosses blood-brain barrier and is most effective drug for PD.
  • Dopamine agonists: stimulate receptors & reduces episodes linked to end-of-dose akinesia .
  • MAO-B Inhibitors: Inhibits specific enzyme that breaks down dopamine
  • COMT-inhibitors: Prevents breakdowns of Levodopa ensuring drug reaches the brain
  • Amantadine: antiviral that helps reduce dyskinesia when using high dosages
• Common Problems and Side Effects: _Gastrointestinal irritation can treat adding carbidopa. Cardiovascular & Arrythmias cautions in Cardiac Pt. Behavior can result in confusion /impulsiveness/depression. Involuntary movements and continuous decreased drug can become less effective.

Dementia and Alzheimer's Disease

• Loss of neurons is thought to be due to the breakdown of several processes necessary for sustaining brain cells with Dementia/Alzheimer’s.
• There's a progressive build up of insoluble fibroid amyloid and disruptions in major neurotransmitters, namely cholinergic abnormalities
• Hallmark symptoms of dementia consist of memory changes & late Alzheimer’s present with incontinence
• Dramatic verbal, emotional, or physical outbursts may also be experienced by those with Alzheimers between 40-60%
• The inability to recal early symptoms and social situations and disorders in sleep are indications of clinical presentation for this disease.

Traumatic Spinal Cord & Brain Injuries

• Spinal Cord Injuries (SCIs) are named according to the level of neurologic impairment, complete lesions loss of sensory and motor function below the level of the lesion, spinal cord transection, severe compression, or vascular dysfunction.
• Mechanism of Injury may be Concussion(blow or shaking, temporary loss), Contusion(spinal cord surface with loss of central gray matter);or Laceration/Maceration resulting from glia disruption. General Clinical Manifestations-loss of paralysis,Autonomic and Orthostatic(hypotension, impaired bowel), Pain, Respiratory Dysfunction

Traumatic Brain injuries:

_is defined as negative affects on brain with external physical force. _Open-breached leaving brain open/closed head not skull fracture/ Penetrative with vascular injury

Minor Traumatic Brain Injury (mTBI) Concussion-is defined as relative or no loss of consciousness within a short time period

_ Symptoms: Dizziness, Disorientation, Nausea, Headache

Cerebrovascular Accident-

Is defined as a medical emergency when there’s a restricted or reduction of blood supply affecting oxygen. Consisting either Ischemic Stroke(clots obstruct vessel causing blood reduction)/ or Hemorrhagic stroke within ruptures of or Transient Ischemic (mimic stroke symptoms only a few hours)

Types of Cerebral Vascular Injuries:

_Middle Cerebral Artery (MCA): contralateral hemiparesis and sensory deficits arm more involved than leg _ACA(anterior cerebral Artery=same with leg involved more than arm) _Proterior: Memory deficits visual anognisia

How to remember Strokes?

• Follow Fast face/arms/speed and time: (more accurate if you remember) BEFAST balance for issues with vision Medication: (Time of essence) -Anticoagulants/Antiplated with Fibrinolytic therapy

Anticoagulants-

_Used for treatment or venous DVT following joint transplants/prolonged injuries. Reduction for patients wit AF or cardiac issues for blood cot. Including Heprin+ Warfarin and Factor + direct Thrombin Inhibitors

Heparin Treatment:

Main objective: to address DVT and prevent or lessen “almost instantaneous Effect. Some issues is Immune function can lead to Thrombocytopenia w increased risk for blood cloths

Warfarin Alternative-

_Works inhibiting vitamin K with some side effects that heparin used during that time is more effective. Regular monitoring if and or PT is required for clotting.

Thrombin/Angiomaz:

Bind directly with ability to impaied for alternative agents like Hephrin for AF

Factor in Habitators:

_Directly target active four with improvements safety but with low risk of therapy

Antiplatelet:

Aspirin(inhibits enzyme that results in stroke prevention) + ADO Receptor (Also known for PT to maintain platelets or Block ADP receptor),

Glycoprotein:

Block GP essential step to stop that platelet Common S andS: Headaches w increase for bleeding/renal issue or antiplater

Intracerebral Hemorrhage- is defined as source of bleeding within parenchyma, most deadliest for subtype

Results in: Headache(stroke), Vomiting, Confusion

Special Implication:

Therapist can manage safe & effective plans to minimize risks with rigorous skills

Edema and control on this factor;

Requires Mannitol to reduce fluids, along as seizure drugs (phenytoin) to minimize swelling or Thrombolistic in patient Use stockings or pneumonia to reduce issues

• Rehabilitation: The specialist should recognize risk and reduce risks of both medication if anti hypertensive/ Diabetic patients can provide safe action during rehabilitation sessions

Imaging of Head/Heart

CT vs MRI:: The similarities to MS to help find abnormalities depending on the side effects and areas that are needed, MRI has greater potential and more accurate _CT can only diagnose Hemorrengh T1 scan for brighter matters / T2 is bright When to Use Imaging Choice? Follow Dr order but check that what’s the purpose of the situation to pick that certain one Follow Acute -subcacute and or CH

Ischemic/stroke:

_CT helps diagnose as the blood clot embolis will be shown. When Edema starts to produce that affect it turns dark.

Heart and cerebral

Help diagnose Emboli for blood flow vessel or vasospasms with small lesions being dense. Then can show swelling side effects after it passes.

Sclerosis

Help show Demyelinated to know the spread and affect while also ruling out commonalities

Ather/ Dementia-

Help see the affects on enlarged ventricle and the size the brain has shrunk to