Neuro Exam 3 - Neuro Slides PDF

Innervation Pattern Remember Brainstem and spinal cord injuries that cause damage to lower motor neuron (LMN) result in findings ipsilateral to the site of damage Anatomical Marking Internal Anatomy The spinal cord consists of An outer ring of white matter (ascending and de...

Innervation Pattern Remember Brainstem and spinal cord injuries that cause damage to lower motor neuron (LMN) result in findings ipsilateral to the site of damage Anatomical Marking Internal Anatomy The spinal cord consists of An outer ring of white matter (ascending and descending fibers) A butterfly-shaped central gray area Dorsal horns contain sensory nerve cells that receive bodily sensory information Ventral horns contain the motor neurons that send motor impulses from the CNS to the muscles The fibers from both the dorsal and anterior roots merge to form a spinal Tracts of the Spinal Cord -- Ascending (Sensory) Transmit sensory information from various body parts The sensory impulses are pain, thermal sensation, touch, proprioception, and kinesthesia Spinal Motor Control Circuitry Lower motor neuron The output pathway to innervate a skeletal muscle Called the final common pathway The efferent impulses from the motor cortex pass through this motor neuron before they can produce a muscle movement Motor unit Consists of four components Motor cell body Efferent fibers Motor end plate aka neuromuscular junction Innervated muscle fibers A motor unit can fire repeatedly, resulting in sustained shortening of the muscle fibers Damage to the LMN cell or the beginning axon Tracts of the Spinal Cord -- Descending Pyramidal tracts Extrapyramidal tracts Tracts of the Spinal Cord -- Descending (Motor) Pyramidal tracts Corticospinal tracts Lateral corticospinal tract Constitutes 90% of the corticospinal fibers Cross midline at the medulla Regulate voluntary muscle activity of the limbs A lesion causes Profound, bilateral weakness Anterior corticospinal tract Constitutes 10% of the corticospinal fibers Descend ipsilaterally and cross before synapsing on the ventral horn Responsible for proximal muscles like those of the trunk Tracts of the Spinal Cord -- Descending (Motor) Extrapyramidal tracts Tectospinal tract Regulates neck and body twisting movements for the startle reflex Rubrospinal tract Regulates muscle muscle tone to support the body against gravity Vestibulospinal tract Regulate reflexive adjustments of body posture Tracts of the Spinal Cord -- Descending (Motor) Extrapyramidal tracts Reticular descending tracts Regulate respiration, vomiting, and cough reflexes Respiration Motor nuclei from C3-C5 Phrenic nerve Innervates the diaphragm https://www.youtube.com/wat ch?v=i43OVrwhW\_E Motor nuclei from T1-T2 Innervates the internal and external intercostal muscles Motor nuclei from T6-T12 Innervates the abdominal muscles Motor Nuclei of the Spinal Cord Spinal gray matter contains motor nerve cells Anterior α- motor neurons Control muscle contraction involved in voluntary movement γ- motor neurons Control muscle contraction in response to external forces acting on the muscle Results in the involuntary, reflexive movement called the stretch reflex Together these nerve cells form Ventral roots of spinal nerves Lower motor neurons Interneurons are neither sensory or Motor Functions of the Spinal Cord Reflexive motor responses A stereotyped and involuntary motor reaction in response to sensory stimulation Independent of cortical voluntary control Reflexes are Influenced indirectly by descending impulses from the motor cortex and brainstem motor centers Input from higher motor centers provides a homeostatic state of motor control, resulting in smooth motor movements If released from higher levels of motor control, the spinal cord reflexes become hyperactive Spinal Reflexes Stretch reflex Tendon-jerk reflexes Knee jerk https://www.youtube.com/watch?v= 6\_wsNvZtcA4 Similar reflexes of the biceps, triceps, quadriceps, and ankle muscles Withdrawal/Flexor Reflex Crossed Extensor Reflex Clinical Correlates -- Altered Reflexes Three patterns of altered reflexes Hyperreflexia Common in UMN disorders https://www.youtube.com/watch?v =iV\_a2WSbdM8&t=1s https://www.youtube.com/watch?v=i 7ed7Kumiv0 Clonus reflex Marked by a repeated contraction followed by relaxation of the muscle during a stretch reflex https://www.youtube.com/watch?v= 4SrhgjGIZ30 Hyporeflexia/areflexia Common in LMN disorders Types of Spinal Cord Disorders Segmental Lesion at a specific spinal level Below that level, sensory and motor functions are impaired Complete spinal transection All sensory and motor functions are lost bilaterally below the lesion All sensory and motor functions are spared above the lesion Types of Spinal Cord Disorders Longitudinal Selectively affects specific nerve cells May impair both sensory and motor systems Spinal hemisection What would you expect to see? Lower Motor Neuron Syndrome Muscle fibers are disconnected from motor efferents Cannot receive Descending cortical impulses Reflexive sensory input Affected muscle fibers gradually atrophy Clinical signs of LMN include Flaccid paralysis Absent reflexes Muscular fibrillation Eventually severe atrophy (wasting) of the muscle involved Cerebellar Anatomy The cerebellum consists of Two hemispheres Internal white matter Four pairs of embedded nuclei Three cerebellar peduncles Cerebellar Lobes Each cerebellar hemisphere is divided into three transverse lobes Anterior aka paleocerebellum Responsible for muscle tone and walking posture Monitors and modifies muscle tone to maintain equilibrium Cerebellar Lobes Each cerebellar hemisphere is divided into three transverse lobes Posterior aka neocerebellum Concerned with the sequential planning and coordination of muscles in the cortically-directed skilled movements Speaking Writing Dancing Flocculonodular aka archicerebellum aka vestibulocerebellum Concerned with equilibrium and conjugated eye movements Longitudinal Cerebellar Regions Three longitudinal regions Vermal Most medial Contributes to body posture Paravermal Located on the either side of the vermis Associated with the regulation of movements of ipsilateral extremities Lateral The outermost portion of the lobe Regulates or adjusts skilled movements of the ipsilateral extremities Cerebellar Peduncles Three cerebellar peduncles Inferior Middle Superior Connect the cerebellum to the brainstem All afferent and efferent fibers traveling to and from the cerebellum pass through these fiber bundles Cerebellar Peduncles (Continued) Inferior cerebellar peduncle Mediates sensorimotor information from the spinal cord and brainstem Mediates vestibular input Middle cerebellar peduncle Mediates ongoing sensorimotor information from the opposite cerebral hemisphere Superior cerebellar peduncle Transmits cerebellar outputs to the motor cortex and spinal cord Mediates ongoing movements Cerebellum Also known as the "little brain" Functions Motor control Movement execution Motor learning Motor memory Cognitive functions Attention Language Emotional control Motor Control -- Motor Execution The cerebellum does not initiate motor activity Integrates sensory information with motor information to coordinate and modify the tone, speed, and range in the execution of skilled motor functions Cerebellar participation is vital to the control of rapid muscular activities that require sequential muscle coordination and ongoing modifications to the motor plan The more precise and skilled the activity, the greater cerebellar Motor Control -- Motor Learning and Motor Memory Motor learning begins with a conscious control of skilled movement through repetition and sensorimotor adjustment With repetition, conscious regulation of the tactile motor activities is no longer required Motor memory Patients with cerebellar pathology Lose movement automaticity (motor memory) Revert back to the stage of conscious controlling of tactile motor patterns Primary Motor Characteristic of Cerebellar Damage -- Ataxia Lack of order and coordination in muscle activities Ataxia is the results of dysmetria, dysdiadochokinesis, and decomposition of movement Ataxic gait Ataxic dysarthria Ataxic Gait Characteristics Marked by disequilibrium Stance and gait are usually broad- based Inability to complete tandem gait tasks https://www.youtube.com/watch?v =py6KwGixTfk Truncal instability may lead to falls Steps may be irregularly placed Legs are lifted too high and slapped to the ground https://www.youtube.com/watch Ataxic Dysarthria Characteristics Slow Slurred Disjointed with irregular articulation breakdown Scanning verbal output Each word or syllable is spoken individually https://www.youtube.com/watch?v =7BnGxeMAM\_s Secondary Motor Characteristic of Cerebellar Damage -- Intention Tremor Results from the impaired ability to dampen accessory movements during a motor act Tremor becomes more severe as the target is approached https://www.youtube.com/watch? v=mBr1ZZ1dr3E Secondary Motor Characteristic of Cerebellar Damage -- Hypotonia & Impaired Checks and Rebounding Decreased muscle tone The muscle becomes floppy Pendulousness An extremity, allowed to swing freely in a pendular manner has a greater than average number of oscillations before coming to rest Impaired check and excessive rebound Impairment in the ability to predict, stop, or adjust the movement https://www.youtube.com/watch?v= \_SiZLBQPHGk Assessment of Cerebellar Function Tasks Tandem gait Finger-to-nose test Rapid sequential movements Alternating motion rates Unaided standing Limb rebounding Examining for nystagmus Hopping Cerebellar Pathologies CVA Vertebrobasilar artery serves as the source of blood to all three cerebellar arteries Posterior inferior cerebellar Anterior inferior cerebellar Superior cerebellar Toxicity Acute toxicity Chronic alcoholism Cerebellar Pathologies Progressive Cerebellar Degeneration Friedreich ataxia The most common progressive degenerative hereditary syndrome An autosomal recessive genetic condition Characterized by Ataxia (incoordination) Progressive imbalance (unsteadiness in walking) Dysarthria Tremor Weakness Loss of proprioception Nystagmus Dysmetria Scanning (segmented and carefully articulated) speech https://friedreichsataxianews.com/201 Clinical Correlates Three identifying characteristics of lateralized cerebellar lesions An ipsilateral character to the signs Deficits related to motor functions with no sensory loss and/or paralysis Patients with cerebellar pathology cannot precisely control their body parts during movement But may have strength and somatosensation Gradual natural recovery, unless the lesion is progressive, massive, or bilateral in nature Basal Ganglia Anatomy Striatum Caudate nucleus A large C-shaped structure with a massive pear- shaped head and a long curved tail Putamen a half-moon--shaped nucleus Globus pallidus Wedge-shaped Claustrum A slender mass of gray matter Connected with sensory cortical areas and contributes to visceral functions and sensory integration Related structures Substantia nigra Subthalamic nucleus Function of the Basal Ganglia Motor regulation BG nuclei do not initiate motor activity BG nuclei refine cortically generated movements by suppressing competing movements, extraneous to precise and focused target motor activity BG nuclei adjust associated automatic motor movements (arm swinging during locomotion, follow-through during throwing, facial expressions, and basic emotional vocalization) Higher mental functions BG nuclei play a role in Processing higher mental functions Regulating personality and emotions Cognition/memory Linguistic functions Innervation Pattern The BG motor organization is contralateral to its sensory input and motor output The BG nuclei communicate to and from the motor cortex on the ipsilateral side, thus influencing the activity of the motor nuclei in the brainstem and spinal cord on the opposite side Therefore, the effects of a BG dysfunctioning are evident on the side of the body contralateral to the lesion There are no LMNs or upper motor neurons (UMNs) in the BG circuitry BG circuitry lesions do not produce the paralysis that is seen after a lesion involving the spinal cord and the primary motor cortex BG nuclei lesions result in a loss of inhibitory influence of motor control precision marked by a released pattern of motor movements that are involuntary Signs of Basal Ganglia Dysfunction Bradykinesia Hypokinesia Akinesia Dyskinesia Athetosis Ballism Chorea Tremor Dystonia Torticollis Myoclonus Bradykinesia, Hypokinesia, & Akinesia Bradykinesia Involves slowness of movement resulting in decreased spontaneity of movement Hypokinesia Involves movement with limited excursion Akinesia Involves impaired movement initiation Dyskinesia -- Athetosis Site of Lesion Globus pallidus and putamen Characteristics Slow, involuntary worm-like twisting of predominantly upper limb and speech muscles Athetosis of the buccofacial muscles causes dysarthria Accompanied by varying degrees of hypertonia in between Movements Dyskinesia -- Tremor Site of Lesion Substantia nigra Characteristics A constantly alternating motor activity in one or more body parts Tremors are divided into two types https://www.youtube.com/watch?v =gAtw2jET9KM Resting tremor Associated with degenerative changes in the substantia nigra Associated with Parkinson disease https://www.youtube.com/watch?v=e 532YW-Zwf0 Intentional, or action, tremor Dystonia -- Torticollis Characteristics An involuntary muscle contraction (spasm) that pulls the body part into an abnormal position https://www.youtube.com/watch? v=2msqI9nCLIg Forms of dystonia Spasmodic torticollis Marked by fixation of the neck Dystonia -- Myoclonus Characteristics Consists of muscle contractions that are isolated and repetitive Result in brief, lightning-like jerks of a body part https://www.youtube.com/watch? v=HeOn99vJ8s0 If the myoclonic jerks interrupt the phasic movements of speech, the patient will present with dysarthria Basal Ganglia Diseases Parkinson disease (PD) Huntington disease (HD) Huntington chorea Wilson Disease Progressive supranuclear palsy (PSP) Tardive dyskinesia (TD) Basal Ganglia Diseases -- Parkinson Disease A progressive condition marked with involuntary tremulous motion with rigidity, and reduced muscular power Cause Degeneration of the cells in the substantia nigra Leads to a dopamine deficiency Statistics Onset of its symptoms occurs between 60 and 70 years of age PD equally affects men and women Characteristics Motor Stooped (forward-bending) posture Festinating gait https://www.youtube.com/watch?v=vsZxnmyBRz0 Tremor at rest Cogwheel rigidity (stiff muscles with cogwheel-like jerk) Bradykinesia (slowed execution of body movements) Loss of postural reflexes (like arm swings) Masked facial expression Micrographia (smaller writing) https://www.youtube.com/watch?v=6IbsJPhREPM Basal Ganglia Diseases -- Parkinson Disease Treatment Pharmacological L -Dopa (Sinemet) has been used to treat patients with dopamine deficiency https://www.youtube.com/watch?v= D7ngF1DFgBs Surgical Deep Brain Stimulation Stimulation of the subthalamic nucleus results in improved motor performance in Parkinson patients Intralaminar centromedianum nucleus stimulation Improved language and other higher mental functions Basal Ganglia Diseases -- Huntington Chorea Huntington disease has three primary characteristics Adult onset Chorea Gradual cognitive deficits in addition to dysarthria Cause HD is an inherited as an autosomal dominant disease Nonspecific atrophy in the caudate nucleus impairing GABA distribution Nonspecific atrophy in the prefrontal and parietal lobes Statistics Affects both men and women equally with symptoms presenting around age 30 Characteristics Motor \*Clumsiness in motor movements Choreiform movements gradually increase Speech becomes dysarthric and gradually deteriorates into muteness Cognitive \*Forgetfulness Basal Ganglia Diseases -- Wilson Disease aka Hepatolenticular Degeneration A progressive disease that results from a disorder of copper metabolism leading to cirrhosis of the liver The diseased liver releases the unmetabolized copper in the blood, which leads to the degeneration of internal brain regions, particularly the BG Cause Autosomal recessive condition caused by a mutation in the copper- transporting gene on chromosome 13q Basal Ganglia Diseases -- Wilson Disease (Continued) Statistics Onset of clinical manifestations is between 10 and 25 years of age Characteristics Motor Increased muscular rigidity Tremor Dysarthric speech, Cognitive Progressive dementia Other Corneal pigmentation (Kayser-- Fleischer ring) is he most important diagnostic attribute Basal Ganglia Diseases -- Progressive Supranuclear Palsy (PSP) A slowly progressive degenerative condition of the brain cells Often confused with other neurodegenerative diseases such as Parkinson Cause Unknown Statistics Incidence is about 1.4 per 100,000 population Affects more men than women Begins between 55 and 70 years of age Average survival from symptom onset to death is about 6 to 7 years Occurs sporadically rather than within Basal Ganglia Diseases -- Progressive Supranuclear Palsy (PSP) Characteristics Motor Lack of balance Bradykinesia (decreased spontaneity in movement initiation) Impaired gait control Supranuclear gaze palsy or loss of voluntary eye movements Rigidity of the trunk and neck Motor speech disorders (dysarthria) https://www.youtube.com/watch?v=HGTFaBi M6GE https://www.youtube.com/watch?v=Qn4VrJ RiBOk Cognitive Forgetfulness Slow thinking Inattention Basal Ganglia Diseases -- Tardive Dyskinesia An acquired motor disorder Cause Results as a side effect from long-term medication treatment given for mental and psychological disorders Characteristics Begins with the emergence of involuntary and repetitive movements involving mouth tongue and facial muscles Facial grimacing Tongue thrust Lip smacking Eye blinking Lip puckering All of which negatively impact motor speech https://www.tardiveimpact.com/what-is-td https://www.youtube.com/watch?v=XnxgfvzTSZ8 Treatment Removal of the medication causing the TD side- Basal Ganglia and Higher Mental Disorders In addition to its role in motor control, the BG has additional roles in emotions, personality, and cognition Caudate pathology has been associated with an acquired deficit in memory related to delayed tasks Basal Ganglia and Psychiatric Disorders BG-based movement disorders and associated neurotransmitter abnormalities are known to have psychiatric concomitants Research suggests that There is a high incidence of depression in patients with Parkinson disease Patients with Huntington chorea exhibit a high suicide rate along with personality and mood disorders. There is an Important connection between the neurotransmitter dysfunctions in movement disorders and psychiatric illnesses Schizophrenia Depression Anatomy of the Motor Cortex Primary Motor Cortex (PMC) Located in the precentral gyrus Organization Homunculus Lower third of the motor cortex represents oral--facial speech muscles and head The face and mouth occupy a disproportionately large cortical area Upper motor cortical region represent the arms and trunk Midsagittal area represents the legs and toes Blood Supply Lateral cortical surface is served by the middle cerebral artery Midsagittal extension of the motor cortex is served by the anterior cerebral artery Cortical Motor System Connections PMC depends on constant feedback from adjacent cortical and subcortical regions Cortical input Supplementary motor cortex (SMA)/ Premotor cortex (PreMC) Regulates planning and implementation of bilateral aspects of movements Sets up a motor plan of a skilled movement pattern involving specific limbs Prefrontal cortex Adds the quality of judgment, foresightedness, and cognitive accountability to motor movements Somatosensory association cortex Regulate higher-order spatial aspects of the movement plan. Subcortical input Basal ganglia Refine cortically generated movements by suppressing competing movements, extraneous to Innervation Pattern Efferent projections from the motor cortex cross the midline at the medulla to innervate contralateral cranial nerve and spinal output motor nuclei A lesion of the descending fibers above the point of decussation produces motor signs contralateral to the site of damage A lesion below the decussation point, clinical motor signs of the spinal lesion are ipsilateral to the locus of the damage. Descending Efferent Tracts/Pyramidal Tracts Corticospinal tract Contains 30% of the motor fibers Mediates voluntary movements of the skeletal muscles through connection with LMNs Corticonuclear tract aka corticobulbar tract Contains the remaining 70% of the motor fibers This is a short tract Controls the facial, oral, and other speech related muscles through activation of brainstem cranial nerve nuclei Virtually all descending fibers in both tracts cross the midline before synapsing on their Corticospinal Tract Motor neural impulses that travel in the corticospinal tract originate from three areas PMC 25% to 30% of the pyramidal tract fibers are known to arise from the PMC PreMC Approximately 30% of the descending motor fibers arise from the PreMC Primary sensory cortex and somatosensory association cortex The remaining 40% of the motor fibers arise from the PSC and the adjacent somatosensory association cortex Corticospinal Tract (Continued) After crossing, the motor fibers descend into the lateral corticospinal tract of the spinal cord Regulate voluntary muscle activity of the limbs Participates in digital control of the skeletal muscles of the distal limbs (fingers and toes) required for fine manipulative skills Corticonuclear/Corticobulbar Tract The motor fibers of the corticonuclear tract cross at various locations in the brainstem and synapse with the motor nuclei of the cranial nerves Trigeminal (CN V) Facial (CN VII) Glossopharyngeal (CN IX) Vagus (CN X) Spinal accessory (CN XI) Hypoglossal (CN XII) An important clinical point about the corticonuclear system is that the muscles of the jaw, larynx, and upper face receive projections from the bilateral motor cortices As a result, a unilateral cortical lesion does not profoundly impair the function of some cranial nerves Facial (CN VII) Trigeminal (CN V) Terms Related to Motor Function Common clinical terms associated with cortical motor dysfunctions Paralysis Defined as loss of voluntary muscle movement Types Monoplegia (paralysis of a single limb) Hemiplegia (paralysis of one side of the body involving both upper and lower limbs) Triplegia (paralysis of any three limbs) Paraplegia (paralysis of both lower limbs) Quadriplegia (paralysis of all four limbs---two upper and two lower) Clinical Correlates -- Pseudobulbar Palsy Pseudobulbar Palsy aka supranuclear paralysis of bulbar nerves Site of Lesion Bilateral involvement of the corticonuclear pathways Injuries to the LMNs in the brainstem, which relate to the motor functions of the cranial nerve Vagus (CN X) Facial (CN VII) Hypoglossal nerves (CN XII) Common causes Degenerative conditions Stroke Neoplasm Characteristics Paralysis of the oral--facial muscles resulting in Dysphagia Difficulty phonating Dysarthria Facial emotional response pattern remains intact Pseudobulbar affect Often exaggerated emotional responses are accompanied by excessive laughter or sobbing https://www.youtube.com/watch?v=9af7ZRyPlLM https://www.ispot.tv/ad/7XH\_/pba-facts-learn-more-featuring-danny-glover https://www.youtube.com/watch?v=Uk7MdKMfypM Clinical Correlates -- Alternating/Crossed Hemiplegia Site of Lesion Brainstem lesions A lesion on one side of the brainstem affects The ipsilateral cranial nerve motor nuclei The uncrossed descending fibers of the corticospinal tract Thus a brainstem lesion can interrupt both the LMN and UMN systems Common causes Stroke Characteristics Alternating pattern of symptoms LMN Ipsilateral pharyngeal, lingual, facial UMN Contralateral spastic hemiplegia Clinical Correlates -- Spastic Hemiplegia Spastic hemiplegia A state of paralysis with hypertonia, hyperreflexia, and spasticity Site of Lesion UMN component of the corticospinal tract Presentation of symptoms Contralateral to the site of lesion Common causes Cerebrovascular accidents Tumors Degenerative diseases of the nervous system Characteristics Clasp-knife rigidity https://www.youtube.com/watch?v=8xxe2WWWoYI Positive Babinski reflex https://www.youtube.com/watch?v=iV\_a2WSbdM8 Typical posture of spastic hemiplegia consists of A flexed upper arm, thumb, and fingers with the neck bent toward the affected side Clinical Correlates -- UMN Syndrome Upper Motor Neuron Syndrome Site of Lesion Lesions of the descending corticospinal fibers Characteristics Paralysis marked by increased muscle tone (spastic hemiplegia) after several weeks of flaccid paralysis Hyperactive spinal reflexes The paralyzed muscles located contralaterally do not atrophy and reflexes are hyperactive. Altered reflexes Pathological reflexes Positive Babinski reflex