Anatomy: Nervous System & Brain

Cell body (soma): contains nucleus and organelles, main metabolic center. Dendrites: short, branching projections that receive signals (graded potentials). Axon: single long process that conducts action potentials away from cell body. Axon hillock: trigger zone where AP is initiated. Myelin sheath: insulating lipid layer (Schwann cells in PNS, oligodendrocytes in CNS). Nodes of Ranvier: gaps in myelin. Synaptic (axon) terminals: release neurotransmitters.

Sensory (afferent) neurons: carry impulses FROM receptors TO CNS; mostly unipolar. Motor (efferent) neurons: carry impulses FROM CNS TO effectors (muscles/glands); multipolar. Interneurons (association neurons): connect sensory and motor neurons WITHIN the CNS; most abundant neuron type; multipolar. Integration and processing occur at interneurons.

Multipolar: many dendrites, one axon (most common — motor neurons, interneurons). Bipolar: one dendrite, one axon (special senses — retina, olfactory). Unipolar (pseudounipolar): single process branches into peripheral and central branch (sensory neurons in dorsal root ganglia). Anaxonic: no distinguishable axon (found in brain and retina).

Approximately −70 mV (inside negative relative to outside). Maintained by: 1) Na⁺/K⁺-ATPase pump (3 Na⁺ out, 2 K⁺ in — electrogenic), 2) K⁺ leak channels (K⁺ diffuses out, making inside more negative), 3) Large intracellular anions (proteins) trapped inside. The membrane is ~75x more permeable to K⁺ than Na⁺ at rest.

1) Resting state: −70 mV, voltage-gated channels closed. 2) Depolarization: stimulus reaches threshold (~−55 mV) → voltage-gated Na⁺ channels open → Na⁺ rushes in → membrane rapidly depolarizes to ~+30 mV. 3) Repolarization: Na⁺ channels inactivate, voltage-gated K⁺ channels open → K⁺ rushes out → membrane returns toward negative. 4) Hyperpolarization: K⁺ channels slow to close → briefly overshoots to ~−80 mV. 5) Na⁺/K⁺ pump restores ionic gradients.

An action potential either fires completely at full amplitude or not at all. If threshold is reached, the AP propagates without decrement (same strength throughout). Stimulus intensity is coded NOT by AP amplitude but by FREQUENCY of APs (stronger stimulus = more APs per second) and by the NUMBER of neurons recruited.

In myelinated neurons, action potentials 'jump' from one Node of Ranvier to the next (saltatory = 'to jump'). Myelin insulates the axon, preventing current leak between nodes. This is much faster (up to 120 m/s) and more energy-efficient than continuous conduction in unmyelinated fibers (~1 m/s). Demyelination (e.g., multiple sclerosis) impairs saltatory conduction.

1) AP arrives at presynaptic terminal. 2) Voltage-gated Ca²⁺ channels open → Ca²⁺ enters. 3) Ca²⁺ triggers synaptic vesicle fusion with membrane (exocytosis). 4) Neurotransmitter released into synaptic cleft. 5) NT binds receptors on postsynaptic membrane. 6) Ion channels open/close → postsynaptic potential (EPSP or IPSP). 7) NT removed by reuptake, enzymatic degradation, or diffusion.

EPSP (Excitatory Postsynaptic Potential): depolarizes the postsynaptic membrane (makes it more positive, closer to threshold) — typically by Na⁺ influx. IPSP (Inhibitory Postsynaptic Potential): hyperpolarizes the postsynaptic membrane (makes it more negative, away from threshold) — typically by Cl⁻ influx or K⁺ efflux. Summation of EPSPs and IPSPs at the axon hillock determines if an AP fires.

Temporal summation: rapid, successive EPSPs from ONE presynaptic neuron accumulate before the first dissipates — reaching threshold. Spatial summation: simultaneous EPSPs from MULTIPLE presynaptic neurons converge on one postsynaptic neuron — their combined effect reaches threshold. Both types can also involve IPSPs, potentially canceling excitation.

Released at: neuromuscular junctions (skeletal muscle), preganglionic neurons of ANS (both sympathetic and parasympathetic), postganglionic parasympathetic neurons, and some CNS pathways. Functions: muscle contraction (nicotinic receptors at NMJ), slows heart rate (muscarinic receptors), promotes digestion. Degraded by acetylcholinesterase (AChE). Deficiency linked to Alzheimer's disease and myasthenia gravis.

Catecholamine neurotransmitter synthesized from tyrosine. Major pathways: 1) Nigrostriatal (substantia nigra → basal ganglia): motor control — degeneration causes Parkinson's disease. 2) Mesolimbic/mesocortical: reward, motivation, pleasure — implicated in addiction and schizophrenia. 3) Tuberoinfundibular: inhibits prolactin release. Excess dopamine linked to schizophrenia; deficiency to Parkinson's and depression.

Monoamine neurotransmitter derived from tryptophan. ~90% is in GI tract (regulates motility); remainder in CNS. Functions: mood regulation, sleep-wake cycles, appetite, pain perception, temperature regulation. Low serotonin linked to depression and anxiety. SSRIs (selective serotonin reuptake inhibitors) are first-line antidepressants — block serotonin reuptake → increase synaptic serotonin.

Catecholamine neurotransmitter and hormone. In CNS: regulates alertness, attention, mood (locus coeruleus). In PNS: primary NT of postganglionic sympathetic neurons — 'fight or flight' responses (increases HR, BP, bronchodilation, pupil dilation). Also released by adrenal medulla as a hormone. Deficiency linked to depression; excess to anxiety. Reuptake inhibited by SNRIs, tricyclics, cocaine.

GABA (gamma-aminobutyric acid): primary INHIBITORY neurotransmitter in the brain. Opens Cl⁻ channels → hyperpolarization. Benzodiazepines and barbiturates enhance GABA activity (anxiolytic, sedative). Glutamate: primary EXCITATORY neurotransmitter in the brain. Binds NMDA and AMPA receptors → Na⁺/Ca²⁺ influx. Critical for learning and memory. Excess glutamate → excitotoxicity → neuronal death (stroke, epilepsy, neurodegenerative disease).

CNS: brain and spinal cord — integration and command center; protected by bone, meninges, and CSF. PNS: everything outside CNS — cranial nerves (12 pairs) and spinal nerves (31 pairs). PNS divisions: Sensory (afferent) and Motor (efferent). Motor division: Somatic (voluntary, skeletal muscle) and Autonomic (involuntary — sympathetic, parasympathetic, and enteric).

Frontal lobe: motor cortex (precentral gyrus), executive function, personality, Broca's area (speech production), prefrontal cortex (judgment, planning). Parietal lobe: somatosensory cortex (postcentral gyrus), spatial awareness, sensory integration. Temporal lobe: auditory cortex, Wernicke's area (language comprehension), memory (hippocampus nearby). Occipital lobe: primary visual cortex.

Located posteroinferior to the cerebrum. Functions: coordination of voluntary movement, balance, posture, motor learning, fine-tuning motor output. Receives input from proprioceptors, vestibular system, and motor cortex. Compares intended vs. actual movement and adjusts. Damage → ataxia (uncoordinated movement), intention tremor, dysarthria (slurred speech), loss of balance. Does NOT initiate movement.

Midbrain (mesencephalon): cerebral peduncles (motor tracts), superior/inferior colliculi (visual/auditory reflexes), substantia nigra (dopamine, motor control), red nucleus. Pons: relay between cerebrum and cerebellum, pneumotaxic and apneustic centers (breathing). Medulla oblongata: cardiovascular center (HR, BP), respiratory rhythm center, reflex centers (vomiting, coughing, sneezing, swallowing, hiccupping). Decussation of pyramids (motor tracts cross).

Paired egg-shaped nuclei forming most of the diencephalon. Functions as the 'gateway to the cortex' — relays and filters almost ALL sensory information to appropriate cortical areas (EXCEPT olfaction, which goes directly to cortex). Also involved in motor relay, emotion, memory, and arousal. Each sensory modality has a specific thalamic nucleus (e.g., lateral geniculate → visual, medial geniculate → auditory).

Small region below the thalamus forming floor of 3rd ventricle. Master regulator of homeostasis. Controls: body temperature, hunger/thirst/satiety, circadian rhythms (suprachiasmatic nucleus), autonomic nervous system output, emotional responses (via limbic connections). Endocrine: produces releasing/inhibiting hormones for anterior pituitary; synthesizes ADH and oxytocin (stored in posterior pituitary).

Functional group of brain structures involved in emotion, memory, and motivation. Key components: hippocampus (formation of new declarative memories — damage causes anterograde amnesia), amygdala (fear, emotional memory, threat assessment), cingulate gyrus (emotional responses, decision-making), fornix (fiber tract connecting hippocampus to hypothalamus), mammillary bodies (memory relay), septal nuclei (pleasure). Closely linked to hypothalamus and prefrontal cortex.

Deep gray matter nuclei within the cerebral hemispheres: caudate nucleus, putamen (together = striatum), globus pallidus, subthalamic nucleus, and substantia nigra (in midbrain). Functions: regulate and fine-tune voluntary movement, inhibit unwanted movement, motor planning. Use indirect/direct pathways. Dysfunction: Parkinson's disease (loss of dopaminergic neurons in substantia nigra → tremor, rigidity, bradykinesia), Huntington's disease (degeneration of caudate/putamen → chorea).

Gray matter (inner, butterfly/H-shape): neuron cell bodies. Dorsal (posterior) horns: sensory neuron synapses and interneurons. Ventral (anterior) horns: motor neuron cell bodies (lower motor neurons). Lateral horns (T1-L2): sympathetic preganglionic neurons. White matter (outer): myelinated axon tracts. Ascending tracts carry sensory info UP (e.g., spinothalamic, dorsal columns). Descending tracts carry motor commands DOWN (e.g., corticospinal/pyramidal tracts).

I Olfactory, II Optic, III Oculomotor, IV Trochlear, V Trigeminal, VI Abducens, VII Facial, VIII Vestibulocochlear, IX Glossopharyngeal, X Vagus, XI Accessory (Spinal Accessory), XII Hypoglossal. Mnemonic: Oh Oh Oh To Touch And Feel Very Good Velvet AH.

CN I Olfactory: Sensory only. Smell. Passes through cribriform plate of ethmoid. Only cranial nerve that projects directly to cortex (bypasses thalamus). CN II Optic: Sensory only. Vision. Optic chiasm → optic tracts → lateral geniculate nucleus of thalamus → visual cortex (occipital lobe). Tested with visual acuity, visual fields, pupillary light reflex (afferent limb).

CN III Oculomotor: Motor. Moves eye (superior, inferior, medial recti; inferior oblique), raises eyelid (levator palpebrae), parasympathetic to pupil constriction (sphincter pupillae) and lens accommodation (ciliary muscle). CN IV Trochlear: Motor. Superior oblique (depresses and intorts eye; 'SO4'). Thinnest CN, only one exiting posteriorly. CN VI Abducens: Motor. Lateral rectus (abducts eye; 'LR6'). Mnemonic: LR6SO4.

Largest cranial nerve. 3 branches: V1 Ophthalmic (sensory): forehead, upper eyelid, nose. V2 Maxillary (sensory): cheek, upper lip, upper teeth, palate. V3 Mandibular (sensory AND motor): lower face, lower teeth, tongue (general sensation); motor to muscles of mastication (temporalis, masseter, pterygoids). Trigeminal neuralgia = intense facial pain.

Mixed nerve. Motor: muscles of facial expression (smile, frown, close eyes), stapedius. Sensory: taste from anterior 2/3 of tongue. Parasympathetic: submandibular, sublingual salivary glands; lacrimal gland. Bell's palsy = idiopathic CN VII paralysis → unilateral facial drooping, inability to close eye, loss of taste. Upper motor neuron lesion (stroke) spares forehead; lower motor neuron lesion (Bell's) affects entire half.

Sensory only. Two divisions: Cochlear branch — hearing (cochlea → spiral ganglion → cochlear nuclei). Vestibular branch — balance and equilibrium (semicircular canals and otolith organs → vestibular ganglion → vestibular nuclei and cerebellum). Damage → sensorineural hearing loss, vertigo, nystagmus. Acoustic neuroma (vestibular schwannoma) compresses CN VIII.

CN IX Glossopharyngeal: Mixed. Sensory: taste and general sensation from posterior 1/3 of tongue; monitors carotid body (chemoreceptors) and carotid sinus (baroreceptors). Motor: stylopharyngeus (swallowing). Parasympathetic: parotid salivary gland. CN X Vagus: Mixed. Longest CN; wanders to thorax and abdomen. Motor: pharynx and larynx muscles (voice). Parasympathetic: heart (slows HR), lungs (bronchoconstriction), GI tract (increases motility/secretion). Sensory: visceral organs.

CN XI Spinal Accessory: Motor only. Innervates trapezius (shoulder elevation/shrug) and sternocleidomastoid (turns head to opposite side). Tested by shrugging shoulders and turning head against resistance. CN XII Hypoglossal: Motor only. Innervates intrinsic and extrinsic tongue muscles (tongue movement for speech and swallowing). Damage → tongue deviates TOWARD the side of the lesion (due to unopposed contralateral muscles).

1) Receptor: detects stimulus. 2) Sensory (afferent) neuron: transmits impulse to CNS. 3) Integration center: usually interneurons in CNS (spinal cord for spinal reflexes). 4) Motor (efferent) neuron: transmits response from CNS to effector. 5) Effector: muscle or gland that carries out the response. Reflexes are rapid, involuntary, predictable responses. Monosynaptic = no interneuron (e.g., patellar reflex). Polysynaptic = interneurons present (e.g., withdrawal reflex).

Sympathetic ('fight or flight'): thoracolumbar origin (T1-L2). Short preganglionic, long postganglionic fibers. NT: ACh (preganglionic), norepinephrine (postganglionic). Effects: increased HR, BP, bronchodilation, pupil dilation, glycogenolysis, blood to skeletal muscles, decreased digestion. Parasympathetic ('rest and digest'): craniosacral origin (CN III, VII, IX, X + S2-S4). Long preganglionic, short postganglionic fibers. NT: ACh (both). Effects: decreased HR, bronchoconstriction, pupil constriction, increased digestion/secretion, urination.

Heart: increases heart rate (chronotropic) and contractility (inotropic) via β1 receptors. Lungs: bronchodilation via β2 receptors. GI tract: decreases motility and secretion, constricts sphincters. Also: pupils dilate (mydriasis), blood vessels to skeletal muscle dilate (β2), skin/visceral vessels constrict (α1), liver releases glucose, adrenal medulla releases epinephrine and norepinephrine.

Heart: decreases heart rate via vagus nerve (CN X) acting on SA/AV nodes (muscarinic M2 receptors). Lungs: bronchoconstriction, increased mucus secretion. GI tract: increases motility (peristalsis) and secretion, relaxes sphincters. Also: pupils constrict (miosis), stimulates salivation, lacrimation, and urination. Dominates during rest, relaxation, and digestion.

1) Dura mater ('tough mother'): outermost, thick, dense CT. In brain, has two layers (periosteal and meningeal) with dural venous sinuses between. 2) Arachnoid mater: middle, web-like. Subarachnoid space contains CSF. Arachnoid granulations (villi) reabsorb CSF into dural venous sinuses. 3) Pia mater ('gentle mother'): innermost, thin, delicate, adheres directly to brain/spinal cord surface, follows every contour.

CSF is produced by choroid plexuses (ependymal cells) in all four ventricles (~500 mL/day; ~150 mL circulating at any time). Flow: Lateral ventricles → interventricular foramen (of Monro) → 3rd ventricle → cerebral aqueduct (of Sylvius) → 4th ventricle → lateral/median apertures → subarachnoid space → reabsorbed by arachnoid granulations into dural venous sinuses (superior sagittal sinus). Functions: cushions brain (buoyancy), removes waste, transports nutrients/hormones.

Selective barrier formed by tight junctions between endothelial cells of brain capillaries, with astrocyte foot processes reinforcing the barrier. Allows passage of: water, O₂, CO₂, glucose (via GLUT1 transporters), lipid-soluble molecules, and some amino acids. Blocks: most drugs, proteins, bacteria, large molecules, many toxins. Clinically important: limits drug delivery to brain. Absent in some areas (circumventricular organs like area postrema — vomiting center).

Stroke (CVA — cerebrovascular accident): sudden disruption of blood flow to the brain → neuronal death. Ischemic (~87%): blood clot blocks cerebral artery — thrombotic (clot forms in vessel) or embolic (clot travels from elsewhere). Treated with tPA (tissue plasminogen activator) within 4.5 hours. Hemorrhagic (~13%): blood vessel ruptures → bleeding into brain. Often due to hypertension or aneurysm. CT scan first to rule out hemorrhage before giving tPA.

Progressive neurodegenerative disorder caused by loss of dopaminergic neurons in the substantia nigra (part of basal ganglia circuit). Results in dopamine deficiency in the striatum. Cardinal signs: resting tremor ('pill-rolling'), rigidity (cogwheel), bradykinesia (slowness), postural instability. Also: shuffling gait, masked facies (reduced expression). Treated with Levodopa (L-DOPA, dopamine precursor) + carbidopa. No cure.

Autoimmune demyelinating disease of the CNS. Immune system attacks oligodendrocytes and myelin sheath → sclerotic plaques (scars). Disrupts saltatory conduction. Symptoms: relapsing-remitting pattern (most common), optic neuritis, muscle weakness, numbness/tingling, fatigue, coordination problems, bladder dysfunction. Diagnosed with MRI (white matter lesions), CSF analysis (oligoclonal bands), evoked potentials. Treated with disease-modifying therapies (interferons, immunosuppressants).

Most common cause of dementia. Progressive neurodegenerative disease characterized by: amyloid-beta plaques (extracellular), neurofibrillary tangles (hyperphosphorylated tau protein, intracellular), loss of ACh-producing neurons (nucleus basalis of Meynert), brain atrophy. Symptoms: progressive memory loss (hippocampus affected early), confusion, language difficulty, personality changes, inability to perform ADLs. Risk factors: age, ApoE4 gene, family history. Treatments: cholinesterase inhibitors (donepezil), NMDA antagonist (memantine). No cure.

1) Astrocytes: most abundant; form BBB, regulate ion/neurotransmitter concentrations, provide structural support, metabolic support (lactate shuttle). 2) Oligodendrocytes: form myelin in CNS (one cell myelinates multiple axons). 3) Microglia: immune cells of CNS; phagocytize pathogens and debris. 4) Ependymal cells: line ventricles and central canal; ciliated (circulate CSF); choroid plexus ependymal cells produce CSF.

1) Schwann cells: form myelin sheath around PNS axons (one Schwann cell per internode on one axon — differs from oligodendrocytes). Also enclose unmyelinated PNS axons. Aid in nerve regeneration (form regeneration tube after injury). 2) Satellite cells: surround neuron cell bodies in PNS ganglia; provide structural support and regulate nutrient exchange. Similar function to astrocytes in CNS.

Upper motor neuron (UMN) lesion (brain or descending tracts): spastic paralysis, hyperreflexia, hypertonia, positive Babinski sign (upgoing toes), no significant muscle atrophy (disuse only). Lower motor neuron (LMN) lesion (anterior horn cells, ventral roots, or peripheral nerves): flaccid paralysis, hyporeflexia/areflexia, hypotonia, muscle atrophy (denervation), fasciculations. Examples: UMN = stroke, MS; LMN = polio, peripheral nerve injury.

Dorsal column-medial lemniscus: carries fine touch, vibration, proprioception. 1st-order neuron ascends ipsilaterally in dorsal columns → synapses in medulla (gracile/cuneate nuclei) → 2nd-order decussates → medial lemniscus → thalamus (VPL) → 3rd-order → somatosensory cortex. Spinothalamic tract: carries pain, temperature, crude touch. 1st-order enters dorsal horn → synapses → 2nd-order DECUSSATES at spinal cord level → ascends in anterolateral spinothalamic tract → thalamus (VPL) → somatosensory cortex.

A dermatome is the area of skin innervated by the sensory fibers of a single spinal nerve. Clinically important for localizing spinal cord or nerve root lesions. Key landmarks: C5 — lateral arm (deltoid area), C6 — thumb, C7 — middle finger, C8 — little finger, T4 — nipple line, T10 — umbilicus, L1 — inguinal region, L4 — medial leg, L5 — dorsum of foot, S1 — lateral foot/sole, S2-S4 — perineum (saddle area). Shingles follows a dermatomal distribution.

The 'brain of the gut' — a semi-autonomous division of the PNS embedded in the walls of the GI tract. Contains ~100 million neurons organized in two plexuses: myenteric (Auerbach's) plexus between muscle layers (controls motility/peristalsis) and submucosal (Meissner's) plexus (controls secretion and blood flow). Can function independently of CNS but is modulated by sympathetic (inhibits) and parasympathetic (stimulates via vagus) input. Uses many neurotransmitters including serotonin, ACh, NO, and substance P.