Basics of Neuroanatomy and Neurophysiology PDF

Basics of Neuroanatomy and Neurophysiology ASS.PROF/ HOSAM MAGDY METWALLY MSC , PHD IN PT OF NEUROLOGY AND NEUROSURGERY The Central Nervous System (C.N. S) A. INTRACRANIAL PART B. SPINAL PART PYRAMIDAL TRACT  Pyramidal Pathway Origin: 1- 40% from area 4 2- 40% from prem...

Basics of Neuroanatomy and Neurophysiology ASS.PROF/ HOSAM MAGDY METWALLY MSC , PHD IN PT OF NEUROLOGY AND NEUROSURGERY The Central Nervous System (C.N. S) A. INTRACRANIAL PART B. SPINAL PART PYRAMIDAL TRACT  Pyramidal Pathway Origin: 1- 40% from area 4 2- 40% from premotor area 3- 20% from general sensory area (area 3,1,2) Course: 1- In white matter of cerebral hemisphere 2 – In the internal capsule 3- In the midbrain 4- In the pons 5- In the medulla oblongata 6- In the spinal cord Termination Functions: 1- Controlling voluntary motor activity 2- Initiation of fine delicate movement 3- Facilitation of the muscle tone STRETCH REFLEX  Components of the stretch reflex 1. Stimulus: Stretch of the muscle 2. Receptor: Muscle spindle (intrafusal muscle fibers) 3. Afferent: Primary and secondary endings 4. Center: Anterior horn cell 5. Efferent: Motor nerve (Alpha motor fibers) 6. Effector organ: Skeletal muscle (Extrafusal muscle fibers) 7. Response: Contraction of same muscle & inform CNS about muscle length Components of stretch reflex response Dynamic response Static response Stimulus Change in rate of stretch Change in length (maintained (sudden) stretch) Receptor Nuclear bag & chain Nuclear bag & chain Afferent 1ry ending on nuclear bag & 2ry ending on nuclear chain chain Center Alpha AHCs (monosynaptic Alpha AHCs (monosynaptic reflex) reflex) Efferent Alpha motor neuron Alpha motor neuron Response Contraction of stretched Contraction of stretched muslce muslce Example Tendon jerk Muscle tone HEMIPLEGIA DEFINITION OF HEMIPLEGIA Paralysis of one side of the body due to pyramidal tract lesion at any point from its origin in cerebral cortex to the 5th cervical segment (beginning of origin of brachial plexus).  I. Vascular Causes: e.g., Thrombotic, embolic or hemorrhage II- Congenital: e.g., cerebral palsy III- Traumatic: Subdural hematoma IV- Inflammatory, e.g., encephalitis and brain abscess. CAUSES V- Neoplastic: e.g., Brain tumors as Meningioma VI- Degenerative or demyelinating: e.g., multiple sclerosis MS VII. Hysterical: Patient suffers from paralysis in the absence of organic pyramidal lesion  CAUSES: I. Vascular Causes: These are the most common. A. Thrombotic: resulting in cerebral infarction. Vessel wall diseases: Cerebral atherosclerosis (most important) and Vasculitis Blood diseases causing hyper viscosity. Circulation diseases: slow circulation results in thrombosis as Heart failure, Systemic hypotension B. Embolic: resulting in cerebral infarction. The source of embolus may be due to: Heart (commonest): Mitral stenosis with Atrial Fibrillation. Distal vessels: Deep venous thrombosis Rare sources: Lungs or Bones C. Hemorrhagic: Intracranial hemorrhage may be: Intracerebral: the bleeding is in the brain substance & may leak into the ventricles; this is very serious as the blood may compress vital centers. The commonest artery causing intracerebral hemorrhage is the middle cerebral artery. Subarachnoid: the bleeding is in the subarachnoid space. Subdural or extradural: the blood often forms a hematoma. The Causes of Intracranial Hemorrhage are : 1. Hypertension: Commonest cause of intracranial hemorrhage. 2. Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid hemorrhage. 3. Hemorrhagic blood diseases: hemophilia. 4. Anticoagulants. 5. Trauma to the head: commonest cause of subdural Confirmed diagnosis by CT & MRI CLINICAL PICTURE MAY VARY CONSIDERABLY ACCORDING TO: The cause of lesion The site of lesion The onset  A-ACCORDING TO THE CAUSE OF THE LESION As the vascular causes are the commonest in hemiplegia, it is important to differentiate the clinical picture in thrombotic, embolic and hemorrhagic lesions.  B. ACCORDING TO THE SITE OF THE LESION The lesion causing hemiplegia may occur at 3 main levels: 1. Spinal cord. 2. Brain stem. 3. Cerebral. I. SPINAL CORD The lesion is on one side of the cord & is situated between CI & C5 segments, it is caused Mechanism of lesion (MOL): stab wound, disc prolapse, D.S. or tumor resulting in the picture of Brown-Sequard syndrome  Brown-Sequard syndrome characterized by: 1. Ipsilateral hemiplegia. 2. Ipsilateral deep sensory loss. 3. Contralateral superficial sensory , loss for pain & temperature. II. BRAIN STEM The lesion is on one side of the brain stem resulting in the picture of crossed hemiplegia characterized by: 1. Hemiplegia on the opposite side of the lesion. 2. Cranial nerve paralysis of L.M.N, nature on the same side of the lesion. III. CEREBRAL The cerebral lesion might be in one of the following sites: (Cortical-subcortical-capsular) A- Cortical: characterized by one or more of the following: 1. Coma if the lesion is extensive. 2. Convulsions if the lesion is irritative. 3.Contralateral cortical sensory loss if the parietal lobe is involved. 4. Aphasia and agraphia if the lesion is in the dominant hemisphere. B-Subcortical: Same as cortical hemiplegia except that the paralysis is more extensive. C- Capsular: Characterized by the following: 1. Complete hemiplegia associated with U.M.N, facial and hypoglossal paralysis on the opposite side of the lesion. 2. Hemi-hyposthesia on the opposite side of the lesion. 3. No convulsions, aphasia or coma. (Part 2) Hemiplegia  B. ACCORDING TO THE SITE OF THE LESION The lesion causing hemiplegia may occur at 3 main levels: 1. Spinal cord. 2. Brain stem. 3. Cerebral. I. SPINAL CORD The lesion is on one side of the cord & is situated between CI & C5 segments, it is caused Mechanism of lesion (MOL): stab wound, disc prolapse, D.S. or tumor resulting in the picture of Brown-Sequard syndrome  Brown-Sequard syndrome characterized by: 1. Ipsilateral hemiplegia. 2. Ipsilateral deep sensory loss. 3. Contralateral superficial sensory , loss for pain & temperature. II. BRAIN STEM The lesion is on one side of the brain stem resulting in the picture of crossed hemiplegia characterized by: 1. Hemiplegia on the opposite side of the lesion. 2. Cranial nerve paralysis of L.M.N, nature on the same side of the lesion. III. CEREBRAL The cerebral lesion might be in one of the following sites: (Cortical-subcortical-capsular) A- Cortical: characterized by one or more of the following: 1. Coma if the lesion is extensive. 2. Convulsions if the lesion is irritative. 3.Contralateral hemiplegia and cortical sensory loss if the parietal lobe is involved. 4. Aphasia and agraphia if the lesion is in the dominant hemisphere. B-Subcortical: Same as cortical hemiplegia except that the paralysis is more extensive. C- Capsular: Characterized by the following: 1. Complete hemiplegia associated with U.M.N, facial and hypoglossal paralysis on the opposite side of the lesion. 2. Hemi-hyposthesia on the opposite side of the lesion. 3. No convulsions, aphasia or coma. C-ACCORDING TO THE ONSET: Onset & Course: 1. Acute onset & regressive course (vascular, infective & traumatic lesions). 2. Gradual onset & progressive course (neoplastic lesions- tumor). 3. Remittent & Relapsing course (M.S.). Symptoms & Signs: Vary according to the onset: Acute lesions: the clinical picture passes through 2 stages: Stage of flaccidity due to neuronal shock. Stage of spasticity; this is the stage of established hemiplegia. Gradual lesions: the hemiplegia passes directly to the stage of spasticity. I. Stage of flaccidity =Flaccid Paralysis =Shock Stage: It lasts from 2 - 6 weeks, the shorter the duration the better the prognosis. This stage is prolonged by general poor condition of the patient's health, infections (e.g., chest or urinary tract infection) & bed sores. S&S are: 1. Complete Absence of Voluntary Movement: The affected limb(s) show no voluntary movement due to severe muscle weakness. 2. Hypotonia: The muscles are extremely soft and floppy due to reduced muscle tone. (Flaccid paralysis) 3. Absence of Reflexes: Tendon reflexes may be absent & no plantar response. 4. Drooping of the Face: The facial muscles on the affected side may appear droopy, leading to an asymmetrical appearance. 5. Difficulty in Swallowing and Speaking: The patient may have dysphagia (difficulty swallowing) and dysarthria (difficulty speaking). II. Stage of spasticity =Spastic Paralysis=stage of established hemiplegia S&S are: 1-weakness of one side of the body. 2-Hypertonia (spasticity). 3-Deep reflexes (exaggerated of normal and appearance of pathological) 4. Lost superficial reflexes. 5. Reappear/Unmask the primitive reflex 6.-Gait. II. Stage of spasticity =Spastic Paralysis=stage of established hemiplegia, (in-details) 1-weakness of one side of the body: It affects the progravity more than the antigravity muscles In U.L: the Extensor are weaker than flexors In L.L: the Flexors are weaker than Extensors 2-Hypertonia (spasticity)=spastic paralysis of the antigravity muscles the paralyzed muscles of clasp-knife type: (This paralysis shows a pyramidal distribution) It affects the antigravity more than the progravity muscles: In U.L. : the flexors are more spastic than the extensors. In L.L. : the extensors are more spastic than the flexors  In both U.L & L.L. the adductors are more spastic than the abductors.  It affects the distal more than the proximal muscles: The hand is spastic than the shoulder. The foot is spastic than the hip. 3-Deep reflexes: Deep reflexes in both U. & L.L. are exaggerated on the paralyzed side (biceps, triceps, and knee & ankle reflexes). Pathological deep reflexes (normally absent) may appear: Finger reflex- patellar reflex- adductor reflex. Clonus may be elicited in the ankle, less frequently in the knee or wrist. (moderate spasticity) 4. Lost superficial reflexes: The abdominal reflex lost on the paralyzed side. Positive Babinski sign: On eliciting the plantar response on the paralyzed side there is dorsiflexion of the big toe with or without fanning of the other toes. 5. Reappear/Unmask the primitive reflex: ASTNR-STNR-TLS-TLP-TLR-TTR-PSR 6.Gait: If the patient can walk, his gait is circumduction due to spasticity of the extensors & adductors of L.L. (Part 3) Hemiplegia Recover of Motor Function: Recovery of motor function after a stroke depends on: Reduction of cerebral edema. Absorption of damaged tissue. Improved local vascular flow. lateral sprouting (plasticity) Shoulder pain and Stroke Short Note Common Causes of Shoulder Pain in stroke: Shoulder subluxation. Impingement syndrome Frozen shoulder. Shoulder hand syndrome. Assessmen planning t Stroke rehabilitation  A. General examination: B- Neurological examination: Include the following: Examination of mental function Examination of speech. Examination of cranial nerves. I)Assessment Examination of motor system. Examination of sensory system. Examination of co-ordination. Examination of postural mechanism. Examination of synergies Examination of gait. Examination of daily living activities (ADL) (Part 4) Hemiplegia  Following the onset of cerebrovascular accident, a state of low tone or flaccidity Flaccid stage exists. The length of this state of flaccidity varies from a short time to period of weeks or months. Decrease the length of this state of flaccidity indicates good prognoses.  Aim of physiotherapy in flaccid stage: Save the patient life (improve respiration, circulation and prevent secondary complication as DVT). Improve postural reaction (trunk control, right reaction, protective reaction, postural tone). Flaccid stage Minimize the effect of tonal abnormality. Increase sensory awareness (orientation of the affected side). Maintain range of motion and prevent secondary complication. Stimulate the muscle on the affected side (encourage active participation of the patient). Preparing the patient for sitting up and standing (early mobility). Improve orofacial function  Methods Save patient life via respiratory exercise, circulatory exercise, improve renal function and care of patient's nutrition Improve postural reaction via improve trunk control and promotion of the developmental higher level in postural reaction including righting, equilibrium and protective. Also prevent or reduce the Flaccid stage primitive reflexes Facilitatory technique: 1. Proprioceptive stimuli; 2. Exteroceptive stimulation 3. Vestibular facilitation Positioning ROM exercises Orofacial training  The goals in spastic stage: Facilitate selectivity (fractionation) Improve postural reactions and trunk control. Minimize the effect of spasticity. The second stage of recovery Increase strength of weak muscles. (Stage of spasticity) Decrease shoulder pain (shoulder hand syndrome) Improve joint proprioception Improve locomotion  Methods Improve fractionation via PNF technique Improve postural reaction via improve trunk control and promotion of the developmental higher level in postural reaction including righting, equilibrium and protective. Also prevent or reduce the primitive reflexes. Inhibitory technique: Spastic stage 1. Proprioceptive inhibition; 2. Local anesthesia 3. Vestibular inhibition Resisted and endurance exercises Decrease shoulder pain Proprioceptive exercises Gait training