NEURO PHYSIO Flashcards
(50 cards)
1
Q
Anatomical divisions of the nervous system
A
- Central Nervous System (CNS): Brain + Spinal Cord.
- Peripheral Nervous System (PNS): Cranial + Spinal nerves.
- CNS handles integration, PNS transmits input/output.
- CNS injury causes widespread effects; PNS lesions are more localized.
Clinical: Used to localize site of neurological lesion.
2
Q
Functional divisions of the nervous system?
A
- Somatic Nervous System: Voluntary control of skeletal muscles.
- Autonomic Nervous System: Involuntary control of viscera.
- ANS has sympathetic (thoracolumbar) & parasympathetic (craniosacral) parts.
- Enteric system considered part of ANS.
Clinical: ANS disorders cause postural hypotension, gastroparesis.
3
Q
Role of the CNS
A
- Processes and integrates incoming sensory input.
- Generates appropriate motor responses.
- Controls higher functions: memory, emotions, cognition.
- Damage leads to paralysis, coma, or sensory loss.
Clinical: CNS damage in stroke, trauma, infections.
4
Q
Role of the PNS
A
- Links CNS with limbs and organs.
- cranial and spinal nerves.
- Transmits afferent (sensory) and efferent (motor) signals.
- Neuropathies affect peripheral nerves.
Clinical: LMN signs like flaccid paralysis, fasciculations seen.
5
Q
autonomic nervous system (ANS)
A
- Controls involuntary functions: HR, digestion, respiration.
- Sympathetic: fight or flight (↑ HR, BP).
- Parasympathetic: rest and digest (↑ GI motility, secretions).
- Regulated by hypothalamus and brainstem.
Clinical: Dysfunction seen in diabetes, Parkinson’s, spinal cord injuries.
6
Q
Synapse & its types ?
A
- Functional junction between two neurons.
- Types: Chemical (NT-mediated), Electrical (gap junctions).
- Chemical: slower, unidirectional; Electrical: faster, bidirectional.
- Presynaptic neuron releases neurotransmitters into cleft.
Clinical: Defective synapses involved in epilepsy, Alzheimer’s.
7
Q
What happens at a chemical synapse
A
- AP arrives at presynaptic terminal.
- Ca²⁺ channels open → Ca²⁺ influx → vesicle fusion.
- NT released into cleft and binds to postsynaptic receptors.
- Postsynaptic potential generated (EPSP/IPSP).
Clinical: Myasthenia Gravis caused by defective ACh receptor.
8
Q
Synaptic delay and its importance
A
- Delay of ~0.5 ms in chemical synapse transmission.
- Due to vesicle fusion, NT release, and receptor activation.
- Absent in electrical synapses.
- Causes slower reflex responses.
Clinical: Increased in demyelinating disorders like MS.
9
Q
Excitatory and inhibitory neurotransmitters
A
- Excitatory: Glutamate (CNS), ACh (NMJ).
- Inhibitory: GABA (brain), Glycine (spinal cord).
- Excitatory NTs cause Na⁺/Ca²⁺ influx → depolarization.
- Inhibitory NTs cause Cl⁻ influx → hyperpolarization.
Clinical: Imbalance leads to seizures, anxiety, movement disorders.
10
Q
Synaptic summation & fatigue
A
- Spatial summation: multiple neurons stimulate one neuron.
- Temporal summation: single neuron fires rapidly.
- Both increase chance of AP generation.
- Synaptic fatigue occurs with prolonged stimulation → ↓ NT.
Clinical: Protective against overstimulation (seen in epilepsy).
11
Q
neurotransmitters & its functionS
A
- Chemicals released to transmit signals across synapses.
- Stored in vesicles; released via Ca²⁺ influx.
- Bind specific receptors (ionotropic/metabotropic).
- Excitatory or inhibitory effects.
Clinical: NT imbalance seen in depression, Parkinson’s, epilepsy.
12
Q
Major excitatory neurotransmitters
A
- Glutamate (main excitatory NT in CNS).
- Acetylcholine (excitatory at NMJ and brain).
- Bind AMPA/NMDA (glutamate) or nicotinic receptors (ACh).
- Promote depolarization and signal propagation.
Clinical: Glutamate excitotoxicity in stroke, ALS.
13
Q
Major inhibitory neurotransmitters
A
- GABA (main brain inhibitor), Glycine (spinal cord).
- Open Cl⁻ channels → hyperpolarization.
- Balance excitatory activity.
- Prevent overactivity (seizure prevention).
Clinical: GABA deficiency → epilepsy, anxiety.
14
Q
What enzymes degrade neurotransmitters?
A
- AChE breaks down acetylcholine.
- MAO breaks down dopamine, serotonin, NE.
- COMT degrades catecholamines in CNS.
- Enzyme inhibitors used therapeutically.
Clinical: AChE inhibitors treat Myasthenia Gravis.
15
Q
Synaptic plasticity
A
- Ability of synapses to strengthen/weaken over time.
- Involves LTP and LTD (long-term changes).
- Important in learning and memory (hippocampus).
- NMDA receptor-dependent.
Clinical: Impaired in Alzheimer’s, cognitive decline.
16
Q
Reflex arc & its components
A
- Receptor → Afferent neuron → CNS → Efferent neuron → Effector.
- Basic functional unit of nervous system.
- Can be monosynaptic or polysynaptic.
- Occurs without conscious control.
Clinical: Used in neuro exams to assess spinal integrity.
17
Q
stretch reflex (myotatic)
A
- Monosynaptic reflex maintaining muscle tone.
- Stimulus: stretch → spindle activation → reflex contraction.
- Example: Patellar (knee jerk) reflex.
- Involves Ia afferents and alpha motor neurons.
Clinical: Hyperactive in UMN lesions, absent in LMN lesions
18
Q
Golgi tendon reflex
A
- Polysynaptic, prevents excessive muscle tension.
- Ib fibers activate inhibitory interneurons.
- Leads to muscle relaxation.
- Opposes stretch reflex.
Clinical: Absent in spasticity due to UMN lesions.
19
Q
Reciprocal inhibition
A
- Inhibition of antagonist during agonist contraction.
- Mediated by inhibitory interneurons.
- Ensures coordinated movements.
- Occurs in all voluntary motor actions.
Clinical: Loss → spasticity in UMN damage.
20
Q
How are reflexes used clinically
A
- Reflex grading: 0 (absent) to 4+ (clonus).
- Reflexes localize spinal segment lesions.
- Superficial reflexes (e.g., abdominal, cremasteric).
- Pathologic reflexes (e.g., Babinski) = UMN lesion.
Clinical: Reflex loss indicates LMN or neuropathy.
21
Q
Major regions of the spinal cord
A
- Cervical, Thoracic, Lumbar, Sacral segments
- Enlargements at cervical & lumbar regions for limb control.
- Central gray matter: H-shaped, with anterior/posterior horns.
- Peripheral white matter: ascending & descending tracts.
Clinical: Lesions localize based on segmental motor/sensory loss.
22
Q
Functional divisions of gray matter
A
- Anterior horn: motor neurons.
- Posterior horn: sensory relay neurons.
- Lateral horn (T1-L2): sympathetic neurons.
- Organized into Rexed laminae (I–X).
Clinical: Anterior horn loss (e.g., polio) → LMN paralysis.
23
Q
Ascending & Descending tracts
A
- Ascending: dorsal columns, spinothalamic, spinocerebellar.
- Descending: corticospinal, rubrospinal, reticulospinal etc
- Tracts organized somatotropically
- Cross at different levels (e.g., medulla, spinal cord).
Clinical: Lesions cause sensory/motor deficits below level.
24
Q
Blood supply of the spinal cord
A
- Ant. spinal artery (supplies ant. 2/3)
- post. spinal artery (supply post. 1/3)
- radicular arteries support lower levels
- artery of adamkewicz supplies lumbar cord
Clinical : ASA sundrome - loss of motor + pain/temp. below lesion
25
Meningeal coverings of spinal cord
- Dura mater: tough outer layer.
- Arachnoid mater: CSF-filled space below.
- Pia mater: innermost layer, adheres to cord.
- Denticulate ligaments anchor cord laterally.
Clinical: Meningitis or trauma may compress spinal structures.
26
Types of sensory receptors
- Mechanoreceptors (touch, pressure).
- Thermoreceptors (temperature).
- Nociceptors (pain).
- Photoreceptors (light), Chemoreceptors (chemical stimuli).
Clinical: Neuropathy affects specific receptors (e.g., vibration in diabetes)
27
Adaptation of sensory receptors
- Slowly adapting: respond continuously (e.g., Merkel, Ruffini).
- Rapidly adapting: respond at stimulus onset/offset (e.g., Pacinian).
- Important for detecting changes vs. sustained stimuli.
- Prevents sensory overload.
Clinical: Dysfunction causes paresthesia or anesthesia.
28
Fine touch and pressure receptors
-- Meissner corpuscles: light touch (fingertips).
- Merkel discs: sustained pressure.
- Pacinian corpuscles: vibration, deep pressure.
- Ruffini endings: skin stretch.
Clinical: Lesions → loss of
discriminative touch.
29
Proprioceptors
- Muscle spindles: muscle length.
- Golgi tendon organs: muscle tension.
- Joint receptors: joint angle, movement.
- Maintain posture, coordinated movement.
Clinical: Impaired in dorsal column damage → ataxia.
30
Lateral inhibition in sensory pathways
- Enhances contrast between stimulated and adjacent areas.
- Sharpens sensory localization.
- Mediated by interneurons.
- Occurs in visual, tactile, auditory pathways.
Clinical: Reduced in CNS lesions → poor discrimination.
31
Types of pain & their fibers
- Fast pain : sharp, localized; A-delta fibers
- Slow pain : dull, aching; C fibers
- Fast pain - neospinothalamic tract
- slow pain -paleospinothalamic tract
Clinical: Fast pain blocked by local anaesthetics; chronic pain in C- fiber dysfunction
32
Pain receptors (nociceptors)
- Free nerve endings in skin and viscera.
- Activated by mechanical, thermal, or chemical stimuli.
- Do not adapt → protective role.
- Bradykinin, histamine, prostaglandins activate receptors.
Clinical: NSAIDs reduce prostaglandins → pain relief.
33
Referred pain
- Pain perceived in area distant from origin.
- Due to convergence of visceral and somatic afferents.
- Ex: MI → left arm pain.
- Brain misinterprets source.
Clinical: Key sign in angina, gallbladder disease, etc
34
Endogenous pain control mechanisms
- Periaqueductal gray → endorphin release.
- Descending serotonin/ norepinephrine pathways inhibit pain.
- Opioid receptors on presynaptic neurons reduce NT release.
- Gate control theory: touch input blocks pain.
Clinical: Basis for TENS, opioids, spinal cord stimulation.
35
Hyperalgesia & Allodynia
- Hyperalgesia: increased pain response to noxious stimuli.
- Allodynia: pain due to normally non-painful stimuli.
- Caused by central/peripheral sensitization.
- Seen in neuropathic pain, fibromyalgia.
Clinical: Managed with anticonvulsants, antidepressants.
36
Dorsal column tracts & their function
- Fasciculus gracilis: lower body.
- Fasciculus cuneatus: upper body.
- Carry fine touch, vibration, proprioception.
- Decussate in medulla (internal arcuate fibers).
Clinical: Lesions → sensory ataxia, positive Romberg sign.
37
Spinothalamic tract
- Anterolateral system: pain, temp, crude touch.
- Neospinothalamic (fast pain) and paleospinothalamic (slow pain).
- Cross at spinal level.
- Synapse in thalamus → sensory cortex.
Clinical: Lesions → contralateral pain/temp loss.
38
Spinocerebellar tract
- Carries unconscious proprioception.
- Dorsal (Clarke’s nucleus) and ventral (double crossing).
- Ends in cerebellum → coordination.
- Ipsilateral conduction.
Clinical: Lesions cause ataxia, especially in Friedreich’s ataxia.
39
How is sensory information organized in the spinal cord?
- Somatotopic: legs medial, arms lateral (dorsal columns).
- Tracts run in predictable anatomical locations.
- Helps lesion localization.
- Some tracts cross, others don’t.
Clinical: Crucial for neurologic diagnosis in spinal cord injury.
40
Brown-Séquard syndrome features
- Hemisection of spinal cord.
- Ipsilateral: motor + dorsal column loss.
- Contralateral: pain/temp loss.
- Due to crossed and uncrossed tract damage.
Clinical: Classic board-level lesion for localization.
41
Thalamus & its role
- Relay station for sensory and motor info.
- All sensory input (except olfaction) goes through thalamus.
- Projects to primary sensory cortex.
- Contains specific relay and association nuclei.
Clinical: Thalamic stroke → contralateral sensory loss, thalamic pain.
42
Nuclei of the thalamus
- VPL: body sensory relay.
- VPM: face sensory relay.
- LGN: visual → occipital cortex.
- MGN: auditory → temporal cortex.
Clinical: Lesions cause specific sensory deficits.
43
Primary somatosensory cortex
- Postcentral gyrus (Brodmann areas 3, 1, 2).
- Receives input from thalamus.
- Organized somatotopically (homunculus).
- Important for localization, intensity of stimuli.
Clinical: Stroke here → loss of contralateral sensory modalities.
44
Association areas of cortex
- Interpret and integrate sensory inputs.
- In parietal, temporal, occipital lobes.
- Important for spatial awareness, recognition.
- Lesions cause agnosias or neglect.
Clinical: Right parietal damage → left hemineglect.
45
Sensory homunculus
- Map of body in sensory cortex.
- Face, hands, lips occupy large areas.
- Reflects receptor density, not size.
- Allows precise localization of sensory input.
Clinical: Used in neurosurgical mapping and lesion correlation.
46
corticospinal tract (pyramidal tract)
Origin: motor cortex → internal capsule → spinal cord.
- 90% fibers cross at pyramids (lateral CST).
- Controls voluntary skilled movement.
- UMN lesion: spasticity, hyperreflexia, Babinski+.
Clinical: Commonly affected in stroke, ALS.
47
Upper vs Lower motor neurons
- UMN: from cortex to spinal cord.
- LMN: from spinal cord to muscle.
- UMN signs: spasticity, clonus.
- LMN signs: flaccid paralysis, fasciculations.
Clinical: Differentiates CNS vs PNS lesions.
48
Extrapyramidal system
- Includes basal ganglia, red nucleus, vestibular & reticular nuclei.
- Involuntary control of posture, tone, coordination.
- Does not pass through pyramids.
- Modulates corticospinal output.
Clinical: Lesions → Parkinsonism, dystonia, chorea.
49
Role of the basal ganglia
- Initiate and modulate motor activity.
- Direct (facilitates) and indirect (inhibits) pathways.
- Dopamine from substantia nigra modulates both.
- Output to thalamus and cortex.
Clinical: Parkinson’s (↓ dopamine), Huntington’s (↓ GABA).
50
Role of the cerebellum in movt.
- Coordinates voluntary movement.
- Maintains balance and posture.
- Compares intended vs actual movement.
- Lesions → ataxia, intention tremor,
dysmetria.
Clinical: Cerebellar signs are ipsilateral to lesion.
