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1. Fundamental Characteristics of Neurons

Neurons possess three fundamental characteristics crucial for their communication and function:

1. Excitability: The ability of a neuron to respond to a stimulus and generate an electrical signal. This means neurons can detect changes in their internal or external environment and convert these changes into electrical impulses. This is the initial step in neural communication.

2. Conductivity: The ability of a neuron to propagate an electrical signal (action potential) rapidly along its plasma membrane from one point to another. Once a signal is generated, it must be transmitted efficiently over potentially long distances within the nervous system.

3. Secretion: The ability of a neuron to release neurotransmitters at its axon terminals in response to an electrical signal. These neurotransmitters diffuse across a synapse and bind to receptors on another cell (neuron, muscle, or gland), thereby transmitting the signal to the next cell.

2. Structure and Function of Neuron Parts

• Dendrites:

  • Structure: Short, branched extensions projecting from the cell body (soma). They are often tree-like in appearance.

  • Function: Primarily the receptive region of the neuron. They receive chemical signals (neurotransmitters) from other neurons and convert them into small electrical changes (graded potentials or postsynaptic potentials) that are then transmitted towards the cell body.

• Axon:

  • Structure: A single, typically long, slender projection extending from the cell body at the axon hillock. It can be myelinated or unmyelinated and branches into axon terminals at its end.

  • Function: The conductive region of the neuron. It specializes in transmitting electrical signals (action potentials) away from the cell body towards other neurons, muscles, or glands.

• Synaptic Vesicles:

  • Structure: Small, membrane-bound sacs located within the axon terminals. They are filled with neurotransmitter molecules.

  • Function: Store and release neurotransmitters into the synaptic cleft upon the arrival of an action potential. This release is crucial for chemical communication between neurons at the synapse.

• Neurofibrils:

  • Structure: Bundles of intermediate filaments (cytoskeletal elements) found within the neuron's cytoplasm, extending into dendrites and axons.

  • Function: Provide structural support to the neuron, maintain its shape, and help in the transport of substances within the cell, particularly along the axon via axonal transport.

3. Brain Tumor Origin

A brain tumor is more likely to have originated from glial cells (e.g., astrocytes, oligodendrocytes, microglia) rather than neurons.

Rationale: This is based on cell biology and proliferation. Neurons are typically postmitotic, meaning they lose their ability to divide and reproduce after reaching maturity. Glial cells, however, retain their capacity for cell division throughout life. Cancer is fundamentally a disease of uncontrolled cell proliferation. Since glial cells can divide, they are much more susceptible to uncontrolled growth and tumor formation. While rare, tumors of neuronal origin (like neuroblastomas) do exist, but glial cell tumors (gliomas) are far more common in the adult brain.

4. Chemically Gated vs. Voltage-Gated Ion Channels

5. Neuron's Resting Membrane Potential (RMP)

A neuron's resting membrane potential (RMP) is the electrical potential difference across the plasma membrane when the neuron is not actively signaling, typically around -70 mV (inside negative relative to outside).

• Ion Concentration Gradients:

  • Na⁺ (Sodium): Much higher concentration outside the cell than inside. This creates a strong electrochemical gradient for Na⁺ to move into the cell.

  • K⁺ (Potassium): Much higher concentration inside the cell than outside. This creates a chemical gradient for K⁺ to move out of the cell, but an electrical gradient (due to the negative RMP) that pulls it back in.

  • Cl⁻ (Chloride): Much higher concentration outside the cell than inside. It contributes to the negative charge inside the cell.

  • Ca²⁺ (Calcium): Much higher concentration outside the cell than inside. It is maintained at very low intracellular levels by pumps.

• State of Gated Channels at Rest:

  • Most voltage-gated Na⁺ channels are closed but capable of opening.

  • Most voltage-gated K⁺ channels are closed but capable of opening.

  • Chemically gated channels are predominantly closed at rest due to the absence of ligand binding.

  • Leak channels (especially K⁺ leak channels) are open, allowing K⁺ to slowly diffuse out of the cell, which is a major factor in establishing the RMP. The Na⁺/K⁺ pump actively maintains these gradients by moving 3 Na⁺ out for every 2 K⁺ in.

6. EPSPs and IPSPs Generation and Threshold Potential

• EPSPs and IPSPs Generation in the Receptive Segment:

  • Excitatory Postsynaptic Potentials (EPSPs): Generated when an excitatory neurotransmitter binds to chemically gated ion channels (e.g., Na⁺ channels or mixed cation channels) on the dendrites or cell body, causing a net influx of positive ions (like Na⁺) into the neuron. This leads to a local, transient depolarization (making the inside less negative) of the postsynaptic membrane.

  • Inhibitory Postsynaptic Potentials (IPSPs): Generated when an inhibitory neurotransmitter binds to chemically gated ion channels (e.g., Cl⁻ channels or K⁺ channels) on the dendrites or cell body. This can lead to an influx of Cl⁻ (making the inside more negative) or an efflux of K⁺ (also making the inside more negative), resulting in a local, transient hyperpolarization or stabilization of the membrane potential. This makes it harder for the neuron to reach threshold.

• Functional Significance of Reaching Threshold Potential at the Initial Segment:

  • The initial segment (axon hillock) is the 'trigger zone' of the neuron, containing a high density of voltage-gated Na⁺ channels. It integrates all the EPSPs and IPSPs received by the dendrites and cell body.

  • If the sum of these graded potentials depolarizes the membrane potential at the initial segment to a critical level (the threshold potential, typically around -55 mV), it triggers an action potential. This is an all-or-none event. Reaching threshold is significant because it's the point of no return for generating a full-blown action potential, which then propagates down the axon to transmit the signal over long distances.

7. Depolarization and Repolarization in the Conductive Segment

These processes describe the phases of an action potential as it propagates along the axon (conductive segment).

• Depolarization: This phase involves the rapid change in membrane potential from negative (resting) to positive.

  • Role of Ion Channels and Ion Movement: When the membrane potential at a given point on the axon reaches threshold, voltage-gated Na⁺ channels rapidly open. This causes a massive and rapid influx of Na⁺ ions into the cell down their electrochemical gradient. The entry of positive Na⁺ ions makes the inside of the membrane briefly positive (reversing the polarity), reaching a peak around +30 mV. As the membrane potential becomes positive, the Na⁺ channels quickly inactivate.

• Repolarization: This phase involves the return of the membrane potential to its negative resting state.

  • Role of Ion Channels and Ion Movement: Shortly after depolarization begins (around the peak of the action potential), the slower-opening voltage-gated K⁺ channels open. Concurrently, the voltage-gated Na⁺ channels inactivate. The opening of K⁺ channels allows K⁺ ions to rapidly exit the cell down their electrochemical gradient. This efflux of positive K⁺ ions causes the inside of the membrane to become negative again. The delayed closing of K⁺ channels can lead to a brief period of hyperpolarization (undershoot) where the membrane potential becomes even more negative than resting, before the Na⁺/K⁺ pump and K⁺ leak channels restore the RMP.

8. Action Potential Propagation: Unmyelinated vs. Myelinated Axons

9. Acetylcholine (ACh) Generating EPSP or IPSP

ACh can generate either an EPSP (excitatory postsynaptic potential) or an IPSP (inhibitory postsynaptic potential) depending entirely on the type of postsynaptic receptor it binds to.

1. ACh generating EPSP: When ACh binds to nicotinic receptors (e.g., at the neuromuscular junction in skeletal muscle or in autonomic ganglia), it causes these ligand-gated ion channels to open. These channels are non-selective cation channels, allowing a net influx of Na⁺ (and a smaller efflux of K⁺) to occur. This influx of positive charge depolarizes the postsynaptic membrane, producing an EPSP and exciting the cell.

2. ACh generating IPSP: When ACh binds to muscarinic receptors (which are G protein-coupled receptors, common in cardiac muscle), the activation of the receptor can lead to the opening of K⁺ channels. The efflux of K⁺ ions hyperpolarizes the postsynaptic membrane, making it more negative. This hyperpolarization makes the cell less likely to fire an action potential, thus producing an IPSP and inhibiting the cell. For example, in the heart, ACh binding to muscarinic receptors slows heart rate by causing hyperpolarization.

10. Meningeal Layers and Spaces (Deepest to Superficial)

1. Pia Mater: Deepest, delicate, highly vascularized layer that directly adheres to the surface of the brain and spinal cord, following all contours (gyri and sulci).

2. Subarachnoid Space: Located between the pia mater and the arachnoid mater. It contains cerebrospinal fluid (CSF) and blood vessels. Arachnoid trabeculae (web-like extensions) span this space.

3. Arachnoid Mater: Middle layer, translucent, avascular membrane. It loosely covers the brain and spinal cord but does not dip into sulci.

4. Subdural Space: A potential space located between the arachnoid mater and the dura mater. It is usually collapsed but can become a real space in pathological conditions (e.g., subdural hematoma).

5. Dura Mater: Most superficial and strongest of the meninges. It is a thick, fibrous, inelastic membrane that forms a tough, protective sac around the brain and spinal cord.

   • In the brain, it has two layers (periosteal and meningeal), which are mostly fused but separate to form dural venous sinuses.

   • In the spinal cord, there is an Epidural Space (between dura mater and vertebral bone), containing adipose tissue and blood vessels. This space is absent in the cranium.

11. Cerebrospinal Fluid (CSF) Flowchart

1. Formation: CSF is formed by the choroid plexuses (specialized capillaries and ependymal cells) located within the ventricles of the brain (primarily lateral, third, and fourth ventricles).

2. Lateral Ventricles: CSF is secreted into the two lateral ventricles.

3. Interventricular Foramina (of Monro): From the lateral ventricles, CSF flows through these foramina into the third ventricle.

4. Third Ventricle: CSF flows through this ventricle.

5. Cerebral Aqueduct (of Sylvius): From the third ventricle, CSF flows through this narrow channel into the fourth ventricle.

6. Fourth Ventricle: CSF flows through this ventricle.

   • Lateral Apertures (of Luschka) and Median Aperture (of Magendie): From the fourth ventricle, CSF exits through these three apertures into the subarachnoid space surrounding the brain and spinal cord.

7. Subarachnoid Space: CSF circulates throughout the subarachnoid space, bathing the entire central nervous system, providing buoyancy, protection, and chemical stability.

8. Arachnoid Villi/Granulations: Excess CSF is reabsorbed into the venous blood circulation via mushroom-shaped extensions of the arachnoid mater called arachnoid villi (or granulations, when macroscopic). These project into the dural venous sinuses (e.g., superior sagittal sinus).

9. Dural Venous Sinuses: CSF drains into these sinuses, becoming part of the venous blood, which eventually returns to the heart.

12. Sensory and Motor Association Areas of the Cerebral Cortex

• Sensory Association Areas:

  • Function: These areas (e.g., somatosensory association area, visual association area, auditory association area) interpret sensory information. They integrate and make sense of raw sensory data received from the primary sensory areas.

  • Contribution to Perception: They allow us to recognize and understand what we are sensing. For example, the visual association area interprets lines, shapes, and colors from the primary visual cortex to recognize an object as a face, or the somatosensory association area allows us to identify an object by touch without seeing it. They store memories of past sensory experiences for comparison and interpretation.

• Motor Association Areas (Premotor Cortex):

  • Function: Located anterior to the primary motor cortex. These areas are responsible for planning and sequencing complex movements. They select and sequence basic motor movements into more complex tasks.

  • Contribution to Movement: They help in the preparation for movement, coordinating the movements of several muscle groups by sending impulses to the primary motor cortex. For example, when you plan to reach for a cup, the premotor cortex orchestrates the sequence of muscle contractions required for that specific action, ensuring smooth and coordinated execution rather than just isolated muscle contractions.

13. Hypothalamus Regulation of Hunger and Thirst

• Regulation of Hunger:

  • The hypothalamus contains nuclei crucial for appetite regulation. The arcuate nucleus is particularly important, containing two sets of neurons with opposing effects:

    • Neuropeptide Y (NPY)/Agouti-related peptide (AgRP) neurons: Stimulate appetite and decrease energy expenditure when activated, leading to increased hunger.

    • Pro-opiomelanocortin (POMC)/Cocaine- and amphetamine-regulated transcript (CART) neurons: Suppress appetite and increase energy expenditure when activated, leading to feelings of fullness.

  • Sensory Inputs: The hypothalamus receives signals from various sources:

    • Hormonal signals: Leptin (released by adipose tissue, reduces hunger), Ghrelin (released by stomach, increases hunger), Insulin (from pancreas, indicates nutrient availability).

    • Nutrient signals: Changes in blood glucose, amino acids, and fatty acids levels are detected.

    • GI tract signals: Stretch receptors in the stomach and hormones like Cholecystokinin (CCK) and Glucagon-like peptide-1 (GLP-1) signal satiety.

• Regulation of Thirst:

  • The hypothalamus contains the thirst center, primarily located in the ventromedial nucleus and the supraoptic nucleus.

  • Sensory Inputs:

    • Osmoreceptors: Located in the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO) (circumventricular organs that lack a blood-brain barrier), these detect changes in extracellular fluid osmolarity. An increase in osmolarity (higher salt concentration) stimulates these receptors, promoting thirst.

    • Baroreceptors: Located in the great vessels and atria, these detect decreases in blood pressure/volume. Lower blood pressure stimulates the release of Angiotensin II, which acts on the SFO to stimulate thirst.

    • Dry mouth/throat: Receptors in the mouth and throat also contribute to the sensation of thirst.

  • Upon stimulation, the thirst center initiates the sensation of thirst and also stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary to conserve water.

14. 12 Cranial Nerves

1. Olfactory Nerve (I): Primary function is smell (sensory).

2. Optic Nerve (II): Primary function is vision (sensory).

3. Oculomotor Nerve (III): Controls movement of four of the six extrinsic eye muscles (medial, superior, inferior rectus, inferior oblique), levator palpebrae superioris (lifts eyelid), and parasympathetic innervation to the iris (pupil constriction) and ciliary body (lens accommodation) (motor).

4. Trochlear Nerve (IV): Controls movement of the superior oblique extrinsic eye muscle (motor).

5. Trigeminal Nerve (V): Major sensory nerve of the face (pain, temperature, touch from face, oral cavity, teeth, meninges) and motor innervation to muscles of mastication (chewing) (mixed).

6. Abducens Nerve (VI): Controls movement of the lateral rectus extrinsic eye muscle (abducts eye) (motor).

7. Facial Nerve (VII): Motor innervation to muscles of facial expression; sensory for taste from anterior two-thirds of tongue; parasympathetic innervation to lacrimal and salivary glands (submandibular and sublingual) (mixed).

8. Vestibulocochlear Nerve (VIII): Primary function is hearing and balance/equilibrium (sensory).

9. Glossopharyngeal Nerve (IX): Sensory for taste from posterior one-third of tongue, general sensation from pharynx; motor to stylopharyngeus muscle (swallowing); parasympathetic innervation to parotid salivary gland; carries sensory signals from carotid sinus (blood pressure) and carotid body (blood O2/$CO2) (mixed).

10. Vagus Nerve (X): Major parasympathetic nerve to thoracic and abdominal viscera (heart, lungs, digestive tract); motor to muscles of pharynx and larynx (swallowing, speech); general sensation from pharynx, larynx; taste from epiglottis; sensory from visceral organs (mixed).

11. Accessory Nerve (XI): Motor innervation to sternocleidomastoid and trapezius muscles (head and shoulder movement) (motor).

12. Hypoglossal Nerve (XII): Motor innervation to intrinsic and extrinsic muscles of the tongue (tongue movements for speech and swallowing) (motor).

15. Path of a Withdrawal Reflex after Touching a Hot Surface

1. Sensory Receptor: Located in the skin (e.g., nociceptor or thermoreceptor) detects the noxious stimulus (heat).

2. An afferent (sensory) neuron transmits the signal (action potential) through the spinal nerve into the spinal cord.

3. Posterior Root: The sensory neuron's axon enters the spinal cord via the posterior (dorsal) root.

4. Posterior Horn: The sensory neuron synapses with an interneuron (or sometimes directly with a motor neuron) in the gray matter of the posterior (dorsal) horn of the spinal cord. Specific cell bodies of sensory neurons are located in the somatic sensory nuclei within the posterior horn.

5. Anterior Horn: The interneuron (or direct synapse) excites a motor neuron whose cell body is located in the somatic motor nuclei within the anterior (ventral) horn of the spinal cord.

6. Anterior Root: The efferent (motor) neuron's axon exits the spinal cord via the anterior (ventral) root.

7. Spinal Nerve: The motor neuron's axon then joins the spinal nerve.

8. Effector: The motor neuron's axon terminates on skeletal muscle fibers (the effector) in the limb, causing them to contract and rapidly withdraw the hand from the hot surface.

16. Decussation in the Nervous System

Definition: Decussation refers to the crossing over of nerve fibers from one side of the central nervous system (CNS) to the other. This typically occurs in the brainstem or spinal cord.

Importance: It is important because it explains why one side of the brain controls movements and sensations on the opposite side of the body. This contralateral control is a fundamental organizational principle of the nervous system. It allows for complex coordination and integration of sensory and motor information.

Specific Example where Decussation Affects Neurological Injury Outcome: The pyramidal tracts (corticospinal tracts), which are responsible for voluntary motor control, largely decussate in the medulla oblongata (specifically, the pyramidal decussation). If a patient suffers a stroke (e.g., ischemic lesion) in the right primary motor cortex of the brain, the injury will result in paralysis or weakness (hemiplegia or hemiparesis) on the left side of the body. This is because the nerve fibers originating from the right motor cortex cross over in the medulla to control muscles on the left side of the body. Conversely, sensory pathways like the spinothalamic tracts (pain and temperature) also decussate in the spinal cord, causing sensory deficits on the contralateral side for injuries to the spinal cord or brainstem.

17. Spinal Nerve Pathway and Splanchnic Nerve Pathway in Sympathetic Innervation

These are two distinct pathways for sympathetic preganglionic axons originating from the thoracolumbar spinal cord to reach their target organs.

1. Fundamental Characteristics of Neurons

Neurons communicate via:

1. Excitability: Respond to stimuli by generating electrical signals.

2. Conductivity: Propagate these electrical signals (action potentials) rapidly along the membrane.

3. Secretion: Release neurotransmitters at axon terminals to transmit signals to other cells.

2. Structure and Function of Neuron Parts

• Dendrites: Branched receptive regions; receive chemical signals, generate graded potentials towards cell body.

• Axon: Long, slender conductive region; transmits action potentials away from cell body.

• Synaptic Vesicles: Membrane-bound sacs in axon terminals; store and release neurotransmitters for synaptic communication.

• Neurofibrils: Cytoskeletal elements; provide structural support and aid axonal transport.

3. Brain Tumor Origin

Brain tumors are more commonly from glial cells than neurons. Rationale: Neurons are postmitotic (lose ability to divide), whereas glial cells retain proliferative capacity, making them susceptible to uncontrolled growth characteristic of cancer.

4. Chemically Gated vs. Voltage-Gated Ion Channels

5. Neuron's Resting Membrane Potential (RMP)

RMP (typically around -70 mV) is maintained by:

• Ion Concentration Gradients: High extracellular Na⁺, Cl⁻, Ca²⁺; high intracellular K⁺.

• State of Gated Channels at Rest: Most voltage-gated and chemically-gated channels are closed. Open K⁺ leak channels are major contributors to RMP.

• Na⁺/K⁺ pump: Actively maintains gradients (3 Na⁺ out, 2 K⁺ in).

6. EPSPs and IPSPs Generation and Threshold Potential

• EPSPs (Excitatory Postsynaptic Potentials): In receptive segment, excitatory neurotransmitters open chemically-gated Na⁺ channels, causing Na⁺ influx and local depolarization.

• IPSPs (Inhibitory Postsynaptic Potentials): In receptive segment, inhibitory neurotransmitters open chemically-gated Cl⁻ or K⁺ channels, causing Cl⁻ influx or K⁺ efflux and local hyperpolarization.

• Functional Significance of Reaching Threshold Potential: The axon hillock integrates these potentials. If depolarization reaches threshold potential (approx. -55 mV), an all-or-none action potential is triggered, propagating the signal.

7. Depolarization and Repolarization in the Conductive Segment

• Depolarization: At threshold, rapid opening of voltage-gated Na⁺ channels causes massive Na⁺ influx, reversing membrane potential to +30 mV. Na⁺ channels then inactivate.

• Repolarization: Slower opening of voltage-gated K⁺ channels leads to rapid K⁺ efflux, returning membrane potential to negative. Delayed K⁺ channel closure can cause brief hyperpolarization before RMP is restored.

8. Action Potential Propagation: Unmyelinated vs. Myelinated Axons

9. Acetylcholine (ACh) Generating EPSP or IPSP

ACh's effect depends on the postsynaptic receptor type:

1. EPSP: When ACh binds to nicotinic receptors (ligand-gated cation channels), it causes Na⁺ influx, leading to depolarization and excitation (e.g., in skeletal muscle).

2. IPSP: When ACh binds to muscarinic receptors (G protein-coupled), it can open K⁺ channels, causing K⁺ efflux, leading to hyperpolarization and inhibition (e.g., slowing heart rate).

10. Meningeal Layers and Spaces (Deepest to Superficial)

1. Pia Mater: Deepest, delicate, vascular, adheres directly to CNS surface.

2. Subarachnoid Space: Contains CSF and blood vessels, between pia and arachnoid.

3. Arachnoid Mater: Middle, avascular, loosely covers CNS.

4. Subdural Space: Potential space between arachnoid and dura.

5. Dura Mater: Superficial, thick, protective outer layer. (Spinal cord also has Epidural Space superficial to dura, containing fat/vessels).

11. Cerebrospinal Fluid (CSF) Flowchart

1. Formation: By choroid plexuses in brain ventricles.

2. Flow: Lateral Ventricles \to Interventricular Foramina (Monro) \to Third Ventricle \to Cerebral Aqueduct (Sylvius) \to Fourth Ventricle.

3. Exit to Subarachnoid Space: Via Lateral (Luschka) and Median (Magendie) Apertures.

4. Circulation: Throughout subarachnoid space.

5. Reabsorption: Via arachnoid villi/granulations into dural venous sinuses.

12. Sensory and Motor Association Areas of the Cerebral Cortex

• Sensory Association Areas: Interpret and integrate raw sensory data, enabling recognition and understanding of perceptions (e.g., recognizing a face, identifying an object by touch). They store sensory memories.

• Motor Association Areas (Premotor Cortex): Plan and sequence complex movements, orchestrating muscle groups for coordinated actions by sending impulses to the primary motor cortex (e.g., planning to reach for a cup).

13. Hypothalamus Regulation of Hunger and Thirst

• Hunger Regulation: The hypothalamus's arcuate nucleus uses NPY/AgRP neurons (stimulate hunger) and POMC/CART neurons (suppress hunger). Receives signals from hormones (Leptin, Ghrelin, Insulin), nutrient levels, and GI tract signals.

• Thirst Regulation: The thirst center (ventromedial, supraoptic nuclei) responds to: Osmoreceptors (in OVLT, SFO) detecting increased osmolarity; Baroreceptors detecting decreased blood pressure; and dry mouth/throat. This initiates thirst and ADH release.

14. 12 Cranial Nerves

1. Olfactory (I): Smell (sensory).

2. Optic (II): Vision (sensory).

3. Oculomotor (III): Eye movements (4 muscles), eyelid lift, pupil constriction (motor).

4. Trochlear (IV): Superior oblique eye muscle (motor).

5. Trigeminal (V): Sensory for face, oral cavity; motor for mastication (mixed).

6. Abducens (VI): Lateral rectus eye muscle (motor).

7. Facial (VII): Facial expression, taste (anterior 2/3 tongue), lacrimal/salivary glands (mixed).

8. Vestibulocochlear (VIII): Hearing, balance (sensory).

9. Glossopharyngeal (IX): Taste (posterior 1/3 tongue), pharynx sensation, swallowing, parotid gland; blood pressure/O2/CO2 signals (mixed).

10. Vagus (X): Major parasympathetic to thoracic/abdominal viscera; swallowing, speech; general/visceral sensation (mixed).

11. Accessory (XI): Sternocleidomastoid and trapezius muscles (head/shoulder movement) (motor).

12. Hypoglossal (XII$$): Intrinsic/extrinsic tongue muscles (speech/swallowing) (motor).

15. Path of a Withdrawal Reflex after Touching a Hot Surface

1. Sensory Receptor detects stimulus.

2. Afferent neuron via spinal nerve into spinal cord via posterior root.

3. Synapses in posterior horn (somatic sensory nuclei) with interneuron.

4. Interneuron excites motor neuron in anterior horn (somatic motor nuclei).

5. Efferent neuron exits via anterior root and joins spinal nerve.

6. Terminates on effector (skeletal muscle), causing withdrawal.

16. Decussation in the Nervous System

Decussation is the crossing over of nerve fibers from one side of the CNS to the other. Its importance lies in explaining contralateral control (e.g., right brain controls left body), vital for coordination. Example: A stroke in the right primary motor cortex leads to paralysis on the left side of the body because pyramidal tracts decussate in the medulla oblongata.

17. Spinal Nerve Pathway and Splanchnic Nerve Pathway in Sympathetic Innervation