Somatic Motor System: Upper and Lower Motor Neurons

Somatic Motor System

• The somatic motor system includes the CNS and PNS components responsible for motor activity.
• Upper motor neurons (UMNs) originate in the primary motor cortex and control voluntary movement.
• UMNs descend, cross (decussate) in the medulla, and synapse with lower motor neurons (LMNs) on the contralateral side.
• Brainstem nuclei influence voluntary movement, muscle tone, and reflex regulation.
• Descending UMN pathways travel through the internal capsule and converge on LMNs.
• UMN lesions result in deficits at the level of the lesion and below.

Decussation

• Decussation occurs in the medulla, where UMN fibers cross the midline in the pyramids.
• Lesions above the decussation cause contralateral symptoms; those below cause ipsilateral symptoms.

Lower Motor Neuron

• Lower motor neurons (LMNs) synapse with UMNs and connect to muscles at the neuromuscular junction (NMJ).
• LMNs, also known as anterior horn cells or alpha motor neurons, have cell bodies in the anterior horn of the spinal cord.
• LMNs exit the CNS to innervate skeletal muscles.
• LMN lesions cause deficits only at the level of the lesion.

Motor System Modulation & Organization

• The thalamus, basal ganglia (BG), and cerebellum modulate the UMN system.
• UMNs exert simultaneous influences on LMNs through parallel operations.
• The motor system is organized according to a homunculus, with the hands disproportionately represented.

Control Systems

• Feedforward control involves anticipation between the motor system and the environment, such as preparing for a bus stop.
• Feedback control requires ongoing sensory input from the body and environment to adjust movements, like reacting to a sudden bus movement.
• Repeated movements become more preprogrammed over time.

Normal Muscle Synergies

• Purposeful movements require synergistic muscle action.
• Coordinated movements utilize reciprocal innervation of agonist and antagonist muscles.
• UMN lesions can disrupt normal synergies, leading to pathological movement patterns.

Motor Activity Types

• Central pattern generators (CPGs) are neural circuits in the spinal cord that simplify routine movements like walking.
• Muscle tone is the resting tension in a muscle.
• Hypertonia is increased muscle tone, while hypotonia is decreased muscle tone (flaccidity).
• Reflexes are stereotyped movements triggered by a peripheral stimulus.
• Voluntary movement is initiated by a conscious decision.

Peripheral Components of the Motor System

• A motor unit consists of a single LMN and the muscle fibers it innervates.
• Type 1 muscle fibers (slow-twitch) are fatigue-resistant and used for sustained activities.
• Type 2b muscle fibers (fast-twitch) are easily fatigued and used for quick, powerful movements.
• Type 2a muscle fibers (intermediate) are faster than Type 1 but not as easily fatigued as Type 2b.

Neuromuscular Junction

• The NMJ is a chemical synapse between a motor neuron axon terminal and a muscle fiber sarcolemma, causing muscle contraction.
• Acetylcholine is released at the NMJ, causing an excitatory response in muscle fibers via calcium influx.

Clinical Connections: LMN Syndrome

• Lower Motor Neuron Syndrome results from damage to the LMN cell body or axon.
• LMN damage leads to hyporeflexia, hypotonia, paralysis or paresis, atrophy, denervation (fasciculations and fibrillations), and flaccidity.
• Common causes include herniated discs, polio, and peripheral nerve lesions.

Clinical Conections: UMN Syndrome

• Upper Motor Neuron Syndrome results in hypertonia (spasticity or rigidity), paresis or paralysis.
• Spasticity, common after stroke, MS, SCI, or TBI, is velocity-dependent hypertonia.
• Rigidity, seen with basal ganglia damage, is non-velocity-dependent hypertonia.

Motor Unit Diseases

• Diseases can affect the motor unit at four sites: LMN cell body, axon, NMJ, or muscle fibers.
• Polio is a viral infection of LMN cell bodies, causing weakness, paralysis, atrophy, and decreased reflexes.
• Neuropathies, like those caused by diabetes or AIDP, affect the axon.
• Myasthenia Gravis is an autoimmune disorder affecting acetylcholine receptors at the NMJ, leading to muscle weakness.
• Duchenne muscular dystrophy is a genetic disorder causing weakness and muscle fiber loss.

Specific Diseases

• Post-polio syndrome can occur 20-30 years after polio infection.
• Myasthenia Gravis symptoms include ptosis, diplopia, and difficulties with mastication, swallowing (dysphagia), and speech (dysarthria).
• Myopathies, like Duchenne muscular dystrophy, are hereditary skeletal muscle diseases.
• Amyotrophic Lateral Sclerosis (ALS) involves both LMN (amyotrophy) and UMN (lateral sclerosis) signs, often leading to death within 2-3 years.

Brown-Séquard Syndrome

• Brown-Séquard Syndrome involves damage to one half of the spinal cord.
• Results in ipsilateral flaccid paralysis at the level of the lesion, ipsilateral spastic paralysis below the lesion, ipsilateral DCML loss below the lesion, and contralateral STT loss below the lesion.

Impact of Damage

• Lower motor neuron damage results in ipsilateral flaccid paralysis or paresis and hyporeflexia.
• Upper motor neuron damage results in spasticity and paresis.
• UMN damage is contralateral if above the decussation and ipsilateral if below.

Central Components of Movement

• The cerebral cortex modulates brainstem UMN and LMN activity, selecting the intended goal of movement.
• The primary motor cortex programs movements and sends signals via the spinal cord to LMNs.
• Motor neuron pools in the spinal cord are somatotopically organized: LMNs innervating specific muscle groups are located in the same area of the gray matter.
• Medial areas control proximal muscles, while lateral areas control distal muscles.
• Posterior areas control flexors, and anterior areas control extensors.

Brainstem Tracts

• The rubrospinal tract, originating in the red nucleus, doesn't contribute significantly to movement in humans.
• The vestibulospinal tracts (feedback) control balance and posture.
• The medial vestibulospinal tract controls the neck.
• The reticulospinal tracts (feedforward) coordinate postural stability with voluntary movements.
• The tectospinal tract (feedback) controls reflexive head and neck movements for gaze adjustment.

Spinal Cord Reflexes

• Spinal cord reflexes are involuntary, stereotyped responses to a stimulus.
• The components of a reflex arc are receptor, afferent fiber, reflex center (CNS), efferent fiber, and effector.
• Monosynaptic reflexes, like the stretch reflex, involve one synapse between sensory and motor neurons.

Monosynaptic Reflex

• The stretch reflex is mediated by muscle spindles and is tested via deep tendon reflexes (DTRs).
• Reciprocal inhibition, mediated by interneurons, inhibits antagonist muscle contraction during agonist contraction.

Other Reflexes

• The inverse myotatic reflex, mediated by GTOs, causes autogenic inhibition (agonist relaxation, antagonist contraction).
• The flexion reflex is a withdrawal response to a noxious stimulus, mediated by the spinospinal system.
• The crossed extension reflex involves flexion of one leg and extension of the contralateral leg to maintain balance.
• The Babinski reflex, normal in babies, indicates corticospinal tract damage in adults (great toe extension and splayed toes).
• The clasp-knife phenomenon involves initial free limb movement followed by increased resistance, indicating UMN damage.
• Clonus is involuntary muscle contraction elicited by abrupt dorsiflexion, indicating UMN damage.

Stepping/Central Pattern Generators

• Central pattern generators (CPGs) in nervous system reduce signal complexity needed for purposeful movements.
• CPGs are executed via central motor programs in the spinal cord and brainstem.
• CPG circuits of LMNs cause alternating flexion and extension of hips and knees during gait.
• Descending input activates CPGs, and cortical input is needed for precise ankle dorsiflexion.

Corticospinal/Pyramidal Tract

• The corticospinal/pyramidal tract facilitates conscious, fractionated (fine motor) movement.
• It descends from the cortex, decussates in the pyramids, and synapses with LMNs in the spinal cord.
• 60% originates in the primary motor cortex (Brodmann area 4).
• Other cortical areas include the premotor/supplementary motor cortex (Brodmann's areas 6) and postcentral gyrus (Brodmann area 1,2,3).

Corticospinal Tracts

• The lateral corticospinal tract (LCST) contains 75-90% of corticospinal fibers, crosses in the pyramidal decussation, descends in the contralateral lateral funiculus, and controls fine motor movements.
• The anterior corticospinal tract (ACST) contains smaller, uncrossed fibers and descends in the ventral funiculus.
• The corticobulbar tract is the functional equivalent of the corticospinal tract for the head and neck.

Suprasegmental Control of Reflexes

• Brainstem dampens spinal reflexes via interneuron pools in the gray matter.
• Spinal cord damage increases reflexes.

Tonic Descending Inhibitory Pathway

• The tonic descending inhibitory pathway (TDIP) dampens reflexes from the brainstem to the spinal cord.
• UMN lesions disrupt the TDIP, causing hypertonia.

Clinical Connections: Spinal Shock

• Spinal shock is the motor system's initial response to an acute spinal cord injury (LMN signs).
• It manifests as hypotonia, hyporeflexia, and loss of sensation, reflexive, and voluntary movement below the level of the lesion.
• After the period of spinal shock, UMN signs (spasticity and hyperreflexia) emerge.

UMN and LMN Syndromes:

• UMN Syndrome is caused by cerebral cortex/corticospinal tract damage, resulting in contralateral weakness (if above decussation) or ipsilateral weakness (if below), hypertonia, and hyperreflexia
• LMN Syndrome is caused by damage to the CNS (spinal cord or brainstem) alpha motor neurons or PNS (LMN axons) which results in segmental and ipsilateral weakness, hypotonia, and hyporeflexia

Comparison: UMN vs. LMN

Introduction to Movement

• Reflexive movement is triggered by an external stimulus and involves a pre-programmed response.
• Voluntary movement is internally generated, improved with practice, pre-planned, and goal-directed.
• Structures within the frontal lobe such as, the primary motor cortex (PMC) controls voluntary movement and motor planning
• The muscles are planned by the cerebellum and BG which then assess the message through spinal interneurons before LMNS carry the message to skeletal muscle

Hierarchy of Movement

• Decision-making for movement occurs in the frontal lobe.
• The cerebellum and basal ganglia regulate movement messages.
• Messages are sent down descending tracts and assessed by spinal interneurons.
• LMNs carry the message to skeletal muscle (the "final common pathway").
• Skeletal muscle executes the command.

Frontal Lobe

• The frontal lobe is responsible for motor planning, houses the primary motor cortex (M1), and the precentral gyrus.
• M1 (Broadmann’s Area 4) sends UMNs to the spinal cord and then to LMNs
• The supplementary motor cortex (pre-frontal) is important for planning movement, synergistic/bilateral movement, and postural/visual adjustments.
• Lateral premotor cortex (pre-frontal) orients body and arm to targets, controlling proximal movements for reaching.

Parietal Lobe

• The posterior parietal cortex (PPC) provides sensory guidance and feedback for movement.
• Brodmann’s Areas 5 and 7

Limbic Area

• Mediates emotions, memories, and internally driven behavior as well as cognitive and emotional state for completing task.
• Connects M1 to SMA
• The anterior cingulate and posterior cingulate belong to the limbic area.

Premotor Cortex

• The premotor cortex (Brodmann area 6) includes the lateral premotor area and supplementary motor area (M2).

Cortical Connections

• The primary motor cortex (PMC/M1) receives projections from the primary somatosensory cortex (PSC), posterior parietal cortex (PPC), supplementary motor area (SMA), and cingulate motor areas (CMAs).
• The PMC sends projections to the spinal cord, connecting to LMNs.

Perceptual Action System

• The Perceptual Action System (PAS) recognizes that purposeful movements correlate with the sensory experience of environment.
• Haptic sensing involves object exploration using cutaneous and proprioceptive information.
• Corticomotoneuronal (CM) activation from M1 is needed for rapid, independent finger movements.

Limbic area

• the Anterior Cingulate / Rostral cingulate motor area (CMAr): M3 also the Posterior Cingulate/ Caudal Cingulate Motor Area (CMAc)
• Connects M1 (primary motor cortex) to SMA (supplementary motor area)
• Receives information from the amygdala, signaling stress/threat and signals stress/threat from other environments.
• Cingulospinal projections that terminates in the intermediate gray, influencing LMNS via interneurons.

Reaching and Grasping

• Precision grip (e.g., grasping a needle) is mediated by M1 and the lateral corticospinal tract through individual CM activation.
• Power grip (e.g., holding a hammer) is mediated by non-CM projections.

Cerebellum and Basal Ganglia

• These adjust UMN activity but have no direct connection with LMNs.
• Cerebellar disorders cause uncoordinated walking (ataxic gait).
• Basal ganglia disorders (e.g., Parkinson's) cause a festinating gait.

Cerebellum

• The cerebellum coordinates movement by comparing actual movement to intended movement.

Cerebellum layers include:

• Molecular Layer that's superficial with low neuron density and mainly dendrites as well as inhibitory interneurons
• Purkinje Layer that's middle consisting of purkinje neurons (inhibitory via GABA) cell bodies
• Granular Layer which is the Innermost layer, packed with excitatory granule cells.

Cerebellum blood supply provided by:

• Posterior Inferior Cerebellar Artery (PICA) off vertebral artery, that's most commonly injured in strokes
• Anterior Inferior Cerebellar Artery (AICA) that's off basilar artery.
• Superior Cerebellar Artery that's also located off basilar artery

Cerebellar Peduncles

• The cerebellum's pathways (white matter) include
• Inferior that connects to the SC.
• Middle that connects to pons
• Superior that mainly carries output.

Fibers and Output

• Mossy fibers are fibers (inferior and middle peduncles) that are excitatory and the most numerous. These projects indirectly through granule cells to the Purkinje neurons. These originate from vestibular nuclei (brainstem), SC and cerebral cortex
• Climbing fibers are also Excitatory as well a most direct to Purkinje neurons, these originate from contralateral inferior olivary nucleus.
• Inferior olivary nucleus is a part of the brainstem that is involved in auditory processing and cerebellum mediated learning. ####Cerebellar Output:
• Purkinje neurons may project directly to vestibular nuclei or synapse in deep cerebellar nuclei. The net effect of Purkinje neurons is inhibitory,modulated by mossy and climbing fibers to deep cerebellar nuclei creating an excitatory drive and being sculpted by inhibitory influence of Purkinje neurons

Phylogenetic Terminology

• The archicerebellum (vestibulocerebellum) ensures balance and controls eye movements
• Primary fibers come from ipsilateral CN VIII (vestibulocochlear nerve).
• Secondary fibers are from ipsilateral vestibular nuclei.
• It Influences tone in limbs, trunk, neck, and extraocular eye muscles and assists in regulating the Vestibular ocular reflex (VOR) to eyes focusing when adjusts to head movement.
  • Outputs influence eye movement and postural adjustments.

Lesion of Flocculonodular

• Lesion of flocculonodular lobe leads to wide base of support and disequilibrium Removal of the vestibulocerebellum reduces plasticity of the VOR so it can’t adjust to the damage

#####Unconscious Pathways or Paelocerebellum in relation to Cerebellum

• Paleocerebelluar (Spinocerebellum) is a coordination part of the cerebellum used for evaluation
• Dorsal Spinocerebellar Tract (DSCT) is located T1-L2/3, used for LE and lower trunk and Conveys unconscious proprioception from LE and lower trunk.
• Is tractipsilateral and enter via inferior peduncle, so lesion ipsilateral
• Cuneocerebellar tract (CT) is from UE, neck, and upper trunk and Conveys unconscious proprioception from the UE, neck and upper trunk
• tract is ipsilateral and enter via inferior peduncle
• Ventral Spinocerebellar Tract (VSCT) is uses info from LE where it CROSSES AT SPINAL LEVEL AND TRAVELS CONTRALATERALLY ASCENDS AND CROSSES BACK IN THE MEDULLA/PONS (double decussates)
  • Enters via the superior peduncle for motor commands
• Rostral Spinocerebellar Tract (RSCT) uses the UEs with with sideipsilaterally
  • It Enters cerebellum via superior and inferior peduncles for motor commands
• Trigeminocerebellar projections UsesCN 5ipsilateral from the face ####All tracts connect ipsilaterally. Unilateral lesion, ipsilateral impairments

Cerebrocerebellum

• Cerebrocerebellum is a voluntary movement as well as motor learning
• Originate in the motor and association cortices of the cerebrum via corticopontocerebellar projections VOR: eyes/head move 1:1 ratio + eye hand coordination with eyes + head move same direction
• Damage= in reaching and incoordination of compound finger movements, issue with agonist and antagonist contractions

Clinical Connection

• Medulloblastoma: malignant tumor of the archicerebellum. the tumor Occurs in children from 4-8, with Symptoms of listlessness, vomiting, headaches, and falling as well as Increased intracranial pressure causes papilledema and swelling to optic nerve that can lead to blindness.
• Paleo Cerebellar Syndrome: Is present in humans similarly to chronic alcoholism who have Difficulty to stand and walk against gravity or wide base of support
• Neocerebellar syndrome: Caused by cardiovascular pathology, tumors, MS and degenerative diseases and Characterized by intention tremors, hypotonia, and ataxia

Examination of Coordination

• Finger that can go to nose and heel to shin

Basal Ganglia Nuclei

• The Basal Ganglia Helps regulate muscle contractions, regulates Muscle force and tone as well as regulate sequencing of movements
• The Basal Ganglia Also regulated Regulation of eye movement,Cognitive function that isn't motor,regulation of emotions as well as Working memory that isn't motor
• The Basal Ganglia is connected toParkinsons, Huntingtons and Dystonia.
• Basal Ganglia consists of:

Nuclei of the Basal Ganglia

• Caudate Nucleus (input)
• Putamen (input)
• Globus Pallidus which consists of internal (output) and external (intermediate)
• Subthalamic Nucleus (intermediate)
• Substantial Nigra consisting of pars compacta (intermediate) and pars reticulata (output) of the Basal Ganglia

Loops BG

• Motor- Movement selection and action
• Input is in the cerebral cortex that projects to caudate nucleus & putamen (receiving nuclei) and that the Output is Globus pallidus internus and substantia nigra to the thalamus (relay station) then back to cortex. LOOP
• Oculomotor loop is about regulation of eye movement in the body,

The Role of the Basal Ganglia

• Prefrontal Function: This part regulates the cognition of the body
• Limbic Function : This section is used for emotins.

Disinhibition of Thalamus

• Thalamocortical (VA/VL) projections are excitatory as (thalamus - cortex)
• Projections from BG to thalamus inhibitory.
• “Foot is on the brake”
• If someone wants to move, they have to inhibit BG to thalamus so thalamus can have an excitatory input at the cortex. Turn off inhibitory message for movemnet.

Direct vs. Inter

• The direct pathway of a human's body is excitatory effect that needs to turn off the baseline inhibitory message off
• The direct pathway is Foot off the break
• Dopamine is excitatory Break down of it: Cortex releases Glutamate (+) stimulates striatum and AP sent to GPi. Straitum releases GABA (-) when going to GPi. GABA (-) inhibits GPi. GPi releases GABA (-)as well. Less inhibition.

Movement Disorders

• Loss of dopamine inhibits the thalamus, decreasing motor activity.
• Parkinson’s is loss of dopamine producing cells due to BG lesion

Parkinsons Disease

• Parkinson’s Disease has progressive degenerative disease that is caused by death of neurons in the SNpr than release dopamine that can also includes loss of dopamine producing cells as Cardinal signs are Tremor that's more resting that Bradykinesia, slowness of movement where RIGIDITY happens in postural muscles that are stiff
• In Parkinson's posture is instable and off balance that also includes environment of genetic causes are known Medications are L-Dopa and carbidopa and dopamine agonists as Parkinson's is a fensciating gait.

Huntington's Disease

• Huntington's Disease causes Atrophy of caudate and putamen as well as Characterized by Motor, as well as Cognitive decline leading to demential and typically onset 40-50 and vegetative state within 10-15 years as
  • Loss of GABAergic neurons and reduction of inhibition in the BG circuit also Loss of excitation of the subthalamic nuclei of the indirect pathway

Disorders of the eye movement:

• Ophthalmoplegia : Paralysis of one or more of the extraocular muscles
• Strabismus: Inability to direct both eyes to the same object (lazy eye).Lateral that's due to paralysis of CN IIIMedial that's due to paralysis of CN VI
• Diplopia: Double vision
• Poor depth perception
• Ptosis: Weakness of levator palpebrae superioris muscle

Cranial Nerves Introduction

• The Cranial Nerves are Distributed though brainstem (midbrain, pons, medulla) except CN1 and CN2 where Sensory nuclei more lateral and Motor nuclei more medial
• The nerves are connected through some, Say, Marry Money, But, My, Brother, Says, Big, Brains, Matter, More

CN I (1)

• Cranial Nerve I (Olfactory Nerve) is Special sense of smell no motor that does NOT synpase in thalamus, does not attach to brainstem, no DRG
• Clinical evaluation: test each nostril separately with a familiar scent where Anosmia can occurs if common cold, trauma, and from degenerative disease
• The Neurons of the smell organ are called Bipolar Neurons in olfactory bulbs

CN II (2)

• CN II (Optic Nerve) is Special sensory and it's for vision with are no motor that consists of Retinal ganglion cells from optic nerve
• Clinical Evaluation: that tests with pupillary and consensual reflexes. Shine a light in their eye and both pupils should constrict , really have someone cover up eye and see if they can read

CN III (3)

• CN III (Oculomotor) is motor and innervates motor extraocular muscles which are Superior, inferior and medial rectusas well
• It Elevates eyelid or opens the eye (Levator palpebrae and Pupil constriction/ accommodation when looking somewhere near) with pupillary and consensual reflexes

CN IV (4) Trochlear

• motor innervates superior oblique muscle and controls eye rotation and depression where SO4 is exits posterior side of brainstem by cerebellum
• Axons leaving the trochlear nucleus crossing midline to innervate the opposite side but eye movement is more down and in

CN VI (6):

• CN VI (6)- Abducens motor, innervates the lateral rectus were LR6 is and just to the side

CN V (5) Trigeminal

• Sensory & Motor with 3 branches being ophthalmic, maxillary and mandibular which main job is to find the Sensation.
• Face, head and cornea, Inner oral cavity- jaws, teeth, nose
• Motor- mastication Refelex of being Masseter and afferent limb of corneal (blink) Clinical evaluation: corneal reflex, sensory tests, palpate muscles of mastication, resist jaw opening

CV VII (7)

• VII (Facial Nerve) that is Both Motor of muscles of facial expression and to closes eye efferent
• Sensory: taste and tactile sense anterior ⅔ tongue + innervates lacrimal, salivary and nasal Dysfunction is usually with Bell’s Palsy such as Inflammatory response on nerve and some demyelination Clinical Evaluation: go through facial expressions

CN VIII (8)

• CN VIII (Vestibulocochlear) is Sensory with Vestibular (position and movement of head) andCochlear (hearing
• Clinical evaluation: finger rub for hearing

CN IX (9)

• CN IX (Glossopharyngeal) Sensory that is connected through Soft palate and pharynx with Taste located to the posterior tongue
• Gag and swallow reflex sensory/ afferent portion “Ah” for elevation of both sides of palate uvula Uvula Deviates to the stronger side and is located by Posterior ⅔ of tongue

NV X (10):

• CN X (Vagus) is Both Larynx, heart, and/or lungs, part of gag efferent Clinical Evaluation: Can have hoarseness for of voice and/or increase heart rate

CN XI (11):

• CN XI (Accessory Motor. controls Elevation of shoulder with trap and turn head with SCM that is used for Clinical evaluation that testis resisted head turning and shoulder shrug

CN XII (12):

• CN XII (12) Hypoglossal ,otor that controls motor movement of the tongue where to Stick tongue out, because it deviate toward lesion side because it is weak + slurred speech to Push into check for MMT

Brainstem Structure

• The Midbrain consists of structure of: Colliculi, Cerebral aqueduct, Contains 3rd and 4th ventricle for CSF fluid
• Periaqueductal gray matter surrounds the cerebral aqueduct also hasMedial lemniscus and spinothalamic tract as well as Substantia Nigra (BG) MLF connects the vestibular nuclei to CN 3 and 4 with Crus cerebri descending motor information exits Locus Coeruleus- releases norepinephrine onto the dorsal nuclei of the SC Raphe Nuclei release serotonin onto dorsal nuclei of the SC

The Pons has a 4th ventricle

• The Pons contains a 4th ventricle between the pons and cerebellum that covers CN 5,6,7,8 nuclei with Medial lemniscus and STT for function
• The Modulla has some structure as
• Nucleus gracilis and nucleus cuneatus (DCML) Internal arcuate fibers and medial lemniscus SST Pyramids and pyramidal decussation with Inferior cerebellar peduncle Hypoglossal and vestibular cranial nerves (8 and 12) connections
• The Blood Supply of the brainstem comes through Off vertebral arteries ###PICA and PONS artery
• PICA : Posterior Inferior cerebellar arteries
• Midline Basilar artery

Clinical Connection:

• Lateral Medullary Syndrome or Wallenberg’s Syndrome such Occlusion of the PICA and presents impairments with trigemental nerve and spinothalamic tract (pain and temp, ipsilateral face and contra body) Structures damages: Ipsilateral Horner’s syndrome (meiosis or pupils dilate , ptosis or eye droop and anhidrosis or lack of sweating), Disequilibrium and dysphonia (difficulty speaking, dysphagia) (difficulty swallowing and dysarthria) (difficulty with pronouncing words).
• Locked- in Syndrome with Occlusion of the basilar artery
• Post pons, anterior pons where the ST tracts impaired so sensory and cognition are intract but can’t move your body, Corticospinal and bulbar are also damaged.

Traumatic Brain Injury

• Traumatic Brain Injury (TBI) Immediate, reversible head trauma affecting the frontal and temporal lobes as Influx of Ca in the brain from the stretching/ tearing of axons Symptoms: loss of consciousness, headache, confusion and visual disturbance as well as Causative factor is transient neuronal dysfunction and may cause diffuse axonal shearing

Hematoma Herniation

• Hematoma Herniation is Result from increased intracranial pressure from added blood that is pooling into head Lesion causes a shift of neural tissue as Displacement of structures leads to unconsciouness/ coma which could be caused by hemorrhage, edema, or tumor.

The Basilar Portion consists of:

• Tracts Nuclei

• Tegmentum

• The Tectum ####Ventricles

• Reticular Formation (RF): The main function with complex net that has with throughout cerebellum and higher areas of function in cerebrum to helps motor as well as Autonomic activity, modulation of pain,regulation of consciousness, but mainly consciousness

TBI & Hematomas

• Coup: After hitting the dashboard your head jerks back up.
• Contrecoup: After head hitting dashboard the most effect being from the frontal lobe can occurs Symptoms: loss of consciousness, headache, confusion and visual disturbance where Transiet neuronal dysfunction and may cause diffuse axonal shearing.

Chronic Traumatic Encephalopathy (CTE):

Caused by repeated blows to the head can have degenerative disease
Only diagnosed on autopsy.

• Impulse control problems

• Aggression

• Mood swings that can be associated with TBI in relation with hematomas

• Central Herniation: Has lesion of the cerebrum that pushes the brain downward that causes impaired consciousness

• Temporal Lobe: (tentorial (uncal herniation)): That pushes the uncus medially and compresses midbrain that affects oculomotor control

• Cerebellar (foramen magnum (tonsillar)): Causes the Inferior portion of cerebellum and tonsils go through forman magnum

• Stupor with Sternal rib and achilles is the way to wake some one up that can affect the function of their body

• Disorder of Consciousness results as Lesions in the brainstem or cerebrum such as RF, and RAS and has hepatic and renal failure, infections, hypoxia, meningitis, encephalitis as Coma can causes Profound state of unconsciousness as withDisruption of the RF and brainstem

Vegetative state-

• Complete loss of consciousness but still able to breathe on their own and have a sleep cycle Minimally conscious state- have at least 1 behavioral sign occurs, gestures (yes or no), some intentional movement. Syncope- brief loss of consciousness from a drop in BP Delirium- changes in attention, orientation not related to head trauma

Peripheral Nerves

• Peripheral Nerve lesions results in loss of peripheral distribution pattern where Spinal nerve lesions result in dermatomal and myotomal distributions
• Peripheral Nerve Damage includes sensory function such as sensory dimished etc

Neuropathies-

• Mono: focal dysfunction to a peripheral nerve, such cut on arm as Traumatic myelinopathy: such as loss of myelin at site of injury caused by excessive compression, stretch, vibration, large diameter axons include proprioception, resolves on own, carpal tunnel Traumatic axonopathy:,All axons all sizes, wallerian degeneration, reflexes, sensation and motor function are reduced or absent, muscle atrophy Nerve severance: complete is with severance of the nerve, diminished reflexes, resolves shortly Diabetes: Diabetes :with achilles reflexes S1 diminishes with loss of sensation as well as Pain,glove and stocking syndrome, orthostatic hypotension or balance issues due to prop and foot muscles Guillain Barreis a Virus that has acute rapid onset that starts distal than proximal of demyelination of schwann cells

####Myopathy

• Diseases that affects the proximal muscle that start up being the first sign! Such are Muscular Dystrophy, and drug indued myopathies Gower’s Maneuver- as children try to stand up when they get upright, the kids put their hands on their knees to get themselves upright. MD: duchness Progressive muscular weakness from birth to 6 years includes NMJ connection Myasthenia Gravis NMJ acetylcholine, head and neck most, progressive muscular weakness, autoimmune, dropping eyelid Normal EMG at rest

EMG & NCS

• Nerve Conduction Studies (NCS): e stim of the nerve and record activity distally, if okay then problem may be CNS Electromyography (EMG differentiates between never and muscle disorders and Fibrillation measure.

• Dystonia, with A Disorder that is used for the cause from abnormal postural caused due to sustained and involuntary muscle contractions as well as Dysarthria lesions

####Brainstem

• Locus coerulues produces neuroephipnerie whereas Pedunculopontine nucleus - ach producing nucleus
• The Uncal or central herniation- oculomotor nerve
• Pedunculopontine nucleus- ach producing nucleus

EXTRA

Periaqueductal gray is the midbrain reason that coordinates the somatic and autonomic reactions to pains, threat, and other emotions The Extrapyramidal system of the motor system hierarchy includes the thalamus Most of the CN are not in frontal lobe LR6 and SO4 Swallow 9 and 10