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• Excitability of muscle spindle (Ia afferents)
• Conductivity of nerve
• Contractility of muscle
• The reflex arc: Receptor (muscle spindle) → Afferent (Ia fiber) → Spinal cord → Efferent (alpha motor neuron) → Effector (muscle)

• Transmit impulses from one neuron to another
• Integration of information
• Neurotransmitter release at synapse causes EPSP/IPSP in postsynaptic neuron

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• Protective reflex - withdraws limb from painful stimulus
• Polysynaptic reflex
• Accompanied by crossed extensor reflex (opposite limb extends to support body weight)

• Beta waves - 14-30 Hz, low amplitude, active/alert state
• Alpha waves - 8-13 Hz, relaxed with eyes closed
• Theta waves - 4-7 Hz, drowsiness/children
• Delta waves - 0.5-4 Hz, deep sleep (slow, high amplitude)

• When a person opens eyes or does mental activity, alpha waves are replaced by beta waves
• This suppression of alpha is called alpha block / alpha desynchronization / Berger's effect

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• Detects change in muscle length (stretch)
• Mediates stretch reflex
• Maintains muscle tone
• Ia fibers → monosynaptic reflex; II fibers → polysynaptic

• Primary motor cortex (precentral gyrus, area 4)
• Premotor cortex (area 6)
• Primary somatosensory cortex (postcentral gyrus, areas 3,1,2)

• Motor cortex (area 4): Voluntary movement, contralateral control, somatotopic representation (homunculus)
• Premotor (area 6): Planning and programming movements
• Sensory cortex (areas 3,1,2): Conscious perception of touch, pain, temperature, proprioception

PAGE 66 - CASE HISTORIES

1. Significance of pain and fever: Indicates infection/inflammation - viral infection of spinal cord (anterior horn)
2. Type of lesion: Lower Motor Neuron (LMN) lesion
3. Diagnosis: Poliomyelitis - poliovirus destroys anterior horn cells → flaccid paralysis, hypotonia, areflexia, muscle atrophy, reaction of degeneration, NO sensory loss

1. Neurological abnormality: Complete transection of spinal cord (spinal shock initially → later UMN syndrome)
2. Level of lesion: Cervical cord (all 4 limbs affected, can move shoulders = C5 level spared → lesion at C5-C6 or above C5)
3. Why stretch reflexes hyperactive: After spinal shock resolves, loss of descending inhibitory control from higher centers → UMN lesion → hyperreflexia, spasticity, Babinski sign

PAGE 67 - CASE HISTORIES

1. Diagnosis: Tabes Dorsalis (syphilitic myelopathy) / Subacute Combined Degeneration (B12 deficiency) - posterior column disease
2. Tracts damaged: Posterior (dorsal) columns - Fasciculus gracilis + cuneatus
3. Inco-ordination + loss of posture/passive movement: Posterior columns carry proprioception, vibration, fine touch, 2-point discrimination. Loss → sensory ataxia (worse in dark, positive Romberg's sign), loss of joint position sense

1. Diagnosis: Syringomyelia
2. Why tactile sensibility spared: Touch fibers travel in posterior columns (ipsilateral) which are NOT damaged; pain/temperature fibers cross in anterior commissure which is destroyed by the cavity
3. Site of lesion: Central cord (cavity in central canal area, affecting anterior white commissure at cervical level)
4. Atrophy of small hand muscles: Cavity expanded to destroy anterior horn cells (LMN) at cervical level → wasting + weakness of intrinsic hand muscles

PAGE 68 - CASE HISTORIES

1. Diagnosis: Brown-Séquard Syndrome (hemisection of spinal cord - right side)
2. Side and site of lesion: Right side of spinal cord, at lower cervical level (C8-T1 based on ulnar border involvement + hand muscle wasting)
3. Why touch is normal: Touch has dual pathways - posterior column (ipsilateral) AND anterior spinothalamic tract (crossed) → both must be damaged to lose touch completely; here only one pathway on one side is cut
4. Why pain/temperature lost on LEFT: Spinothalamic tract fibers cross immediately (within 1-2 segments) to the opposite side → right side lesion cuts left-side pain/temperature fibers → contralateral loss

1. Diagnosis: Right-sided internal capsule stroke (CVA) - Upper Motor Neuron lesion
2. Site of lesion: Right internal capsule (or right cerebral peduncle)
   • Contralateral (left) UMN spastic paralysis
   • Tongue deviates to left (ipsilateral to LMN of hypoglossal) but no atrophy → UMN lesion of XII nerve on right
   • Lower face palsy on left = contralateral UMN facial palsy (upper face spared)

PAGE 69 - CASE HISTORY + SPECIAL SENSES

1. Diagnosis: Parkinson's Disease
2. Part of nervous system involved: Basal ganglia - specifically loss of dopaminergic neurons in Substantia Nigra → decreased dopamine in striatum
3. Why movements are few and slow (bradykinesia/akinesia): Dopamine normally inhibits the indirect pathway and facilitates movement. Its loss → overactivity of subthalamic nucleus → excessive inhibition of thalamus → reduced cortical activation → poverty of movement
4. Treatment: Levodopa + Carbidopa (L-DOPA); also dopamine agonists, MAO-B inhibitors

• Taste cells (gustatory receptor cells)
• Supporting cells
• Basal cells
• Taste pore
• Afferent nerve fibers

• Detection of taste (gustation) - sweet, sour, salty, bitter, umami
• Taste pore allows chemicals to contact microvilli of taste cells
• Receptor potential generated → afferent signal via CN VII (anterior 2/3 tongue), CN IX (posterior 1/3), CN X (epiglottis)

PAGE 70 - SPECIAL SENSES + ENDOCRINES

• Detects deep pressure, vibration (high frequency), stretch
• Rapidly adapting mechanoreceptor

• Light touch: Meissner's corpuscle (rapidly adapting)
• Sustained touch/pressure: Merkel's discs (slowly adapting)
• Vibration/deep pressure: Pacinian corpuscle (rapidly adapting)
• Stretch: Ruffini endings (slowly adapting)
• All generate receptor potential → action potential in afferent nerve → spinal cord → thalamus → somatosensory cortex

• Cause: Hypersecretion of Growth Hormone (GH) from anterior pituitary occurring before fusion of epiphyseal plates (pre-puberty)
• Features: Excessive height (>7 feet), organomegaly, enlarged hands/feet, normal proportions
• If GH excess occurs after epiphyseal fusion → Acromegaly (enlargement of acral parts only)