THE NEUROLOGY

Multiple Choice Questions in Neurology: True and False statements about Kennedy Syndrome: CAG repeat Gynecomastia Testicular atrophy Peripheral neuropathy Ocular muscle involvement Kennedy's Disease Inheritance X-linked recessive disorder Trinucleotide repeat: CAG gene Clinical Features Slowly progressive limb-girdle type muscle weakness Slowly progressive bulbar dysfunction Early tremor Muscle cramps Fasciculations Marked abnormal sensory nerve conduction study Degeneration of both motor and sensory neurons Lower motor neurons signs Elevated serum creatine kinase Abnormal sex hormone levels Gynecomastia Testicular atrophy Diabetes mellitus Note: Extraocular muscles are spared. References: Fischbeck, K. H. "Kennedy disease." Journal of inherited metabolic disease 20.2 (1997): 152-158. Sperfeld, Anne D., et al. "X-linked bulbospinal neuronopathy: Kennedy disease." Archives of Neurology 59.12 (2002): 1921-1926. [Answers are A. CAG repeat-True, B. Gynecomastia-True...

High Yield Facts ⭆ Acetylcholine released in postsynaptic cleft and binds to α-subunit of acetylcholine receptor. When acetylcholine bind a nicotinic AchR, a conformational change occurs in the receptor, resulting in the formation of an ion pore. The opening of a ion pore produces a rapid increase in the cellular permeability of sodium and calcium ions, resulting in the depolarisation and excitation of the muscle cell. It activate the sodium channel and depolarizes the nerve fibers. Direction of transmission of nerve impulse from postsynaptic junction to nerve fibers. Question Which of the following ion channel opens, when acetylcholine (ACh) binds to acetylcholine receptor (AChR) at postsynaptic junction? Potassium (K) Chloride (Cl) Calcium (Ca) Sodium (Na) Acetylcholine Receptors Two types of Acetylcholine Receptor: Muscarinic Type: G-Protein Coupled Receptor. Slow metabolic response through intracellular secondary messenger system involving an increase of intracellula...

High Yield Facts ⭆ Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. Motor neurons release acetylcholine (ACh) neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine ionotropic receptors (nAChRs) on the cell membrane of the muscle fiber. The binding of ACh to the receptor can depolarize the muscle fiber, results in muscle contraction. Normally, Acetylcholine (ACh) binds to α-subunit of Acetylcholine Receptor (AChR) at postsynaptic junction. Which ion is responsible for transmission of impulse from postsynaptic junction to nerve fibers? Chloride (Cl) Calcium (Ca) Sodium (Na) Magnesium (Mg)...