Neuroanatomy: Spinal Cord and Motor Control

Innervation Pattern

• Brainstem and spinal cord injuries damaging lower motor neurons (LMNs) result in ipsilateral findings.
• The spinal cord has an outer ring of white matter containing ascending and descending fibers.

Anatomical Marking - Internal Anatomy

• The spinal cord has a butterfly-shaped central gray area.
• Dorsal horns contain sensory nerve cells receiving bodily sensory information.
• Ventral horns contain motor neurons sending motor impulses to muscles from the central nervous system (CNS).
• Fibers from dorsal and anterior roots merge to form spinal tracts.

Tracts of the Spinal Cord - Ascending (Sensory)

• Transmit sensory information from various body parts.
• Sensory impulses include pain, thermal sensation, touch, proprioception, and kinesthesia.

Spinal Motor Control Circuitry

• Lower motor neurons are the output pathway to skeletal muscles.
• Called the final common pathway.
• Efferent impulses from the motor cortex pass through these neurons before muscle movement.

Tracts of the Spinal Cord - Descending (Motor)

• Composed of pyramidal and extrapyramidal tracts.
• Pyramidal tracts (corticospinal tracts) control voluntary limb movements.
• Lateral corticospinal tract constitutes 90% of corticospinal fibers, crossing the medulla.
• Anterior corticospinal tract constitutes 10% of corticospinal fibers, also crossing the medulla.

Tectospinal Tract

• Regulates neck and body movements for startle reflexes.

Rubrospinal Tract

• Regulates muscle tone supporting the body against gravity.

Vestibulospinal Tract

• Regulates reflexive adjustments of body posture.

Reticular Descending Tracts

• Regulate respiration, vomiting, and cough reflexes.
• Involves motor nuclei from C3 to C5.
• Phrenic nerve innervates the diaphragm (C3-C5).
• Other motor nuclei (T1-T2) innervate the internal and external intercostal muscles (T6-T12) and abdominal muscles.

Motor Nuclei of the Spinal Cord

• Spinal gray matter contains motor nerve cells.
• Anterior α-motor neurons control voluntary muscle contraction.
• Anterior γ-motor neurons regulate muscle contraction in response to external forces.

Motor Functions of the Spinal Cord

• Reflexive motor responses are stereotyped, involuntary reactions to sensory stimulation.

Spinal Reflexes

• Reflexes are independent of cortical voluntary control.
• Input from higher motor centers ensures a homeostatic state for smooth motor movements.
• If higher motor control is released, spinal reflexes become hyperactive.
• Stretch reflexes include tendon-jerk reflexes (such as knee jerk) and reflexes of biceps, triceps, quadriceps, and ankle muscles.
• Withdrawal/Flexor reflex.
• Crossed Extensor reflex.

Clinical Correlates - Altered Reflexes

• Three patterns: hyperreflexia (common in upper motor neuron (UMN) disorders), clonus, and hyporeflexia/areflexia (common in lower motor neuron (LMN) disorders).

Types of Spinal Cord Disorders

• Segmental lesions affect a specific spinal level, impairing sensory, and motor functions below the lesion level.
• Complete spinal transection results in bilateral loss of sensory and motor functions below the lesion.
• Longitudinal lesions selectively impact specific nerve cells, possibly affecting both sensory and motor systems.
• Spinal hemisection affects both sensory and motor systems on the ipsilateral side.

Lower Motor Neuron Syndrome

• Muscle fibers are disconnected from motor efferents, resulting in progressively worsening atrophy.
• Signs include flaccid paralysis, absent reflexes, and muscular fibrillation.

Cerebellar Anatomy

• The cerebellum is composed of two hemispheres, internal white matter, and four pairs of embedded nuclei.
• Three cerebellar peduncles (superior, middle, inferior) connect to the brainstem.
• The cerebellum is divided into three transverse lobes (anterior, posterior, flocculonodular).
• The anterior lobe (paleocerebellum) controls muscle tone and posture.
• The posterior lobe (neocerebellum) plans and coordinates skilled movements.
• The flocculonodular lobe (archicerebellum) regulates equilibrium and posture.

Cerebellar Pathologies

• Cerebrovascular accidents (CVAs) can damage the cerebellar arteries (posterior inferior cerebellar artery and anterior inferior cerebellar artery), leading to cerebellar pathologies.

Cerebellar Damage

• Ataxia: Lack of order/coordination in muscle activities, resulting from dysmetria, dysdiadochokinesis, and decomposition of movement, and ataxic gait.
• Ataxic dysarthria: speech characterized by slow, poorly coordinated movements of the articulators.
• Intention tremor: intentional movements that create tremors that increase as the target is approached.
• Hypotonia/impaired check and rebound: reduced muscle tone, difficulty controlling movement amplitude and speed, and excessive rebounding.

Basal Ganglia Anatomy

• Basal ganglia structures include the striatum (caudate nucleus and putamen), globus pallidus, and claustrum.
• Related structures include the substantia nigra and subthalamic nucleus.

Function of the Basal Ganglia

• Motor regulation: Basal ganglia (BG) nuclei refine and suppress competing movements, promoting precise and focused target-directed motor activity, automatic motor movements, emotional expression, and vocalization.
• Higher mental functions: BG nuclei also contribute to processing higher mental functions.

Innervation Pattern (Basal Ganglia)

• BG motor organization is contralateral to sensory input and motor output.
• BG nuclei communicate to and from the motor cortex on the ipsilateral side, influencing the opposite side's brainstem and spinal cord motor nuclei activity.

Signs of Basal Ganglia Dysfunction

• Bradykinesia: slowness of movement.
• Hypokinesia: reduced movement.
• Akinesia: absence of movement.
• Dyskinesia: abnormal involuntary movements (athetosis, ballism, chorea).
• Tremor: involuntary shaking movement.
• Dystonia: sustained or intermittent muscle contractions causing abnormal postures or twisting movements.
• Torticollis: abnormal neck posture.
• Myoclonus: sudden, brief, involuntary muscle contractions.

Basal Ganglia Diseases (Parkinson's Disease)

• Parkinson disease (PD): a progressive neurodegenerative disorder causing movement issues.
• Cause: degeneration of cells in the substantia nigra leading to dopamine deficiency.
• Characteristics include tremor at rest, cogwheel rigidity, bradykinesia, and stooped posture.
• Symptoms may include masked facial expression, loss of postural reflexes, and micrographia.
• Treatment: pharmacological therapies (e.g., levodopa/L-Dopa) and surgical procedures (e.g., deep brain stimulation).

Basal Ganglia Diseases (Huntington's Disease)

• Huntington's disease (HD): an inherited, autosomal dominant disorder causing progressive degeneration of the brain, particularly the basal ganglia.
• Cause: genetic mutation affecting the copper-transporting gene.
• Progressive symptoms include chorea, dysarthria, and cognitive decline, often leading to dementia.
• Characterized by involuntary, irregular movement (chorea) that gradually worsens, affecting speech, cognitive function, and gait.

Basal Ganglia Diseases (Wilson's Disease)

• Wilson's disease (a progressive, autosomal recessive movement disorder), also known as hepatolenticular degeneration.
• Cause: a mutation in the copper-transporting gene on chromosome 13q.
• Characterized by excessive copper in the brain, liver damage, and neurological symptoms such as rigidity, tremor, dysarthria, and cognitive impairment.

Basal Ganglia Diseases (Progressive Supranuclear Palsy)

• Progressive supranuclear palsy (PSP) is a neurodegenerative brain disorder.
• Cause: unknown.
• Characterized by progressive difficulty moving the eyes in normal directions, often to the point of fixed gaze.
• Other symptoms include rigidity, difficulty swallowing (dysphagia), and a lack of balance (ataxia).

Basal Ganglia Diseases (Tardive Dyskinesia)

• Tardive dyskinesia (TD) is an acquired motor disorder.
• Cause: long-term use of certain medications, particularly antipsychotics.
• Characterized by involuntary, repetitive, or rhythmic movements, typically affecting the face, mouth, lips, tongue, and jaw.

Cortical Motor System Connections

• The primary motor cortex (PMC) receives input from other cortical areas and subcortical structures to coordinate and plan movement.
• The supplementary motor cortex (SMA) and premotor cortex are involved in planning and implementing movement.
• The prefrontal cortex affects judgment, cognitive awareness and spatial aspects of movement execution, and the somatosensory association cortex is important for regulating higher-order spatial planning.
• Subcortical structures like the basal ganglia assist in refining movements.

Innervation Pattern (Motor Cortex)

• Motor cortex efferent projections cross the midline at the medulla.
• Lesions above the decussation produce contralateral motor signs, while lesions below produce ipsilateral signs.

Corticospinal Tract

• Contains 30% of motor fibers mediating voluntary skeletal muscle movement through LMN connections. These fibers originate in the primary motor cortex.
• Corticonuclear tract (or corticobulbar) contains 70% and regulates facial, speech, and other cranial nerve-related muscles via brainstem connections. Fibers originate from the motor cortex, passing through the brainstem and synapsing with cranial motor neurons.

Clinical Correlates - Upper Motor Neuron (UMN) Syndrome

• UMN syndromes are often characterized by increased muscle tone (spastic paralysis), hyperactive reflexes, and pathological reflexes (like Babinski).
• The affected muscles do not atrophy as a result of the lesion.

Clinical Correlates – Pseudobulbar Palsy

• A state of paralysis of the oral-facial muscles, with symptoms such as dysphagia (difficulty swallowing) and dysarthria (difficulty speaking), resulting from bilateral lesions of the corticonuclear pathways.

Clinical Correlates - Alternating/Crossed Hemiplegia

• Brainstem lesions affecting both the ipsilateral cranial nerve motor nuclei and uncrossed descending fibers of the corticospinal tract can lead to alternating symptoms, interrupting both LMN and UMN systems. 
• Clinical features involve both ipsilateral cranial nerve deficits and contralateral corticospinal tract deficits, highlighting the brainstem location of the lesion. Example symptoms include hemiparesis, or difficulty with chewing, speaking, and swallowing.

Clinical Correlates – Spastic Hemiplegia

• A state of paralysis marked by hypertonia (increased muscle stiffness), hyperreflexia (excessive reflex responses), and spasticity in the affected limbs, arising from UMN lesions in the corticospinal tract contralateral to the site of damage. The lesion is in the UMN pathway, not LMN pathways.

Test your knowledge on the anatomy and functions of the spinal cord, including the innervation patterns and motor control circuitry. Explore key concepts such as lower motor neurons, spinal tracts, and the sensory pathways involved in bodily sensations.