Neurophysiology

Neurons communicate via rapid changes in membrane voltage called action potentials. The resting membrane potential (RMP) is typically around -70mV, maintained by the Na+/K+ ATPase pump (3 Na+ out, 2 K+ in) and K+ leak channels. A stimulus reaching threshold (~ -55mV) opens voltage-gated Na+ channels, causing rapid depolarisation. This is followed by repolarisation (Na+ channels inactivate, K+ channels open) and transient hyperpolarisation. Myelination by Schwann cells (PNS) or Oligodendrocytes (CNS) enables saltatory conduction at the Nodes of Ranvier, significantly increasing signal speed. Synaptic transmission involves neurotransmitter release (e.g., Glutamate, GABA, Acetylcholine, Dopamine) from the presynaptic terminal, binding to receptors on the postsynaptic cell. The Autonomic Nervous System (ANS) comprises the Sympathetic ('fight or flight', thoracolumbar outflow) and Parasympathetic ('rest and digest', craniosacral outflow) branches, which generally have opposing effects mediated by different receptor types (Adrenergic vs. Muscarinic).

The Nernst equation calculates the equilibrium potential for a single ion, while the Goldman-Hodgkin-Katz equation provides a more accurate RMP considering multiple ions. Action potential velocity is directly proportional to axon diameter and myelination. For example, A-alpha fibres (proprioception) are fast and myelinated, while C-fibres (dull pain) are slow and unmyelinated. At the NMJ, an action potential triggers Ca2+ influx, leading to ACh release. ACh binds to nicotinic receptors, causing depolarisation of the muscle end-plate and muscle contraction. Sensory receptors like Meissner's corpuscles (light touch) and Pacinian corpuscles (vibration/pressure) demonstrate specific adaptations. Motor control involves the primary motor cortex for voluntary movement, basal ganglia for movement initiation/planning, and the cerebellum for coordination and error correction. Reflex arcs, such as the monosynaptic stretch reflex (e.g., patellar reflex), provide rapid, involuntary muscle contraction without cortical input. The Blood-Brain Barrier (BBB), formed by tight junctions between endothelial cells and astrocyte foot processes, protects the CNS from circulating toxins and pathogens.

Demyelinating diseases like Multiple Sclerosis (MS) impair saltatory conduction, leading to slowed or blocked nerve impulses and diverse neurological deficits. Myasthenia Gravis, an autoimmune condition targeting ACh receptors at the NMJ, causes fatiguable muscle weakness. Epilepsy results from abnormal, excessive, and synchronised neuronal activity. UMN lesions typically present with spasticity, hyperreflexia, and extensor plantar responses (Babinski sign); LMN lesions cause flaccid paralysis, atrophy, fasciculations, and hyporeflexia. Autonomic dysfunction (dysautonomia) can manifest as postural hypotension, bladder/bowel dysfunction, or abnormal sweating. Understanding dermatomes and myotomes is crucial for localising spinal cord lesions and nerve root compression.

Nerve Conduction Studies (NCS) measure nerve conduction velocity and amplitude, useful for diagnosing neuropathies. Electromyography (EMG) assesses muscle electrical activity, distinguishing myopathies from neuropathies. Electroencephalography (EEG) records cortical electrical activity, essential for diagnosing and classifying epilepsy. Lumbar puncture (LP) allows CSF analysis for markers of inflammation (e.g., oligoclonal bands in MS), infection, or haemorrhage (xanthochromia in SAH).

Management often targets neurotransmitter systems: e.g., Levodopa for Parkinson's disease (dopamine precursor), SSRIs for depression (serotonin reuptake inhibition), and anticonvulsants for epilepsy (modulating ion channels or GABAergic transmission). Myasthenia Gravis is treated with acetylcholinesterase inhibitors (e.g., Pyridostigmine) to increase ACh availability at the NMJ. Acute UMN pathologies like ischaemic stroke require urgent reperfusion therapies (thrombolysis, thrombectomy) to minimise neuronal damage.