Author: dp

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40. Pseudobulbar palsy

  1. Is a result of a damage of motor fibers traveling from the cerebral cortex to the lower brain stem ?
  2. Is a result of a lower motor neuron lesion of the nerves in the lower brain stem?
  3. Normal emotions?
  4. Labile emotions?
  5. Spastic tongue?
  6. Wasted tongue, fasciculations?

  1. T
  2. F
  3. F
  4. T
  5. T
  6. F

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39. Motor innervation of the upper limb (I)

  1. Biceps brachii:  radial nerve?
  2. Triceps brachii: radial nerve?
  3. Brachioradialis: radial nerve?
  4. Flexor carpi radialis: radial nerve?
  5. Extensor pollicis longus: radial nerve?
  6. Extensor pollicis brevis: radial nerve?

  1. F
  2. T
  3. T
  4. F
  5. T
  6. T

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38. Motor neuron diseases

Upper motor neurons (UMN)
Lower motor neurons (LMN)

  1. Amyotrophic lateral sclerosis (ALS): UMN degeneration + LMN degeneration?
  2. Progressive muscular atrophy (PMA): LMN degeneration?
  3. Primary lateral sclerosis (PLS): UMN degeneration?
  4. Progressive bulbar palsy (PBP): LMN degeneration?
  5. Hereditary spastic paraplegia (HSP): LMN degeneration?
  6. Pseudobulbar palsy: UMN degeneration?

  1. T
  2. T
  3. T
  4. T
  5. F
  6. T

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37. Effects of various drugs on the neuromuscular junction

  1. Pyridostigmine is a reversible acetylcholinesterase inhibitor?
  2. Amifampridine blocks potassium channel efflux in nerve terminals which increases duration of the action potential?
  3. Aminoglycoside antibiotics can aggravate myasthenia gravis (MG) ?
  4. Patients with MG show decreased susceptibility to depolarizing neuromuscular blocking agents ?
  5. Patients with MG show increased susceptibility to non-depolarizing neuromuscular blocking agents?
  6. Patients with Lambert-Eaton myasthenic syndrome show decreased susceptibility to both depolarizing and non-depolarizing neuromuscular blockers?

  1. T
  2. T
  3. T
  4. T
  5. T
  6. F

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36. Brodmann areas

  1. Area 4 – Primary somatosensory cortex?
  2. Area 44, 45 – Auditory cortex?
  3. Areas 3, 1, 2 – Primary motor cortex?
  4. Area 17 – Secondary visual cortex?
  5. Areas 41, 42 – Broca’s area?
  6. Area 18 – Primary visual cortex?

  1. F
  2. F
  3. F
  4. F
  5. F
  6. F

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35. Neuromuscular junction

  1. When action potential arrives at the presynaptic neuron terminal, voltage-dependent calcium channels open and calcium ions flow from the extracellular fluid into the neuron?
  2. Influx of calcium into the neuron triggers the fusion of acetylcholine  vesicles with the membrane and the release of ACh into the synaptic cleft?
  3. Nicotinic and muscarinic ACh receptors (AChRs) are ligand-gated ion channels?
  4. The binding of ACh to nicotinic AChR in the postsynaptic muscle membrane opens a calcium channel within the receptor allowing calcium influx and depolarization of the muscle membrane?
  5. Two ACh molecules must bind with each AChR to open its channel?
  6. Choline acetyltransferase in the synaptic cleft decomposes ACh into choline and acetic acid?

  1. T
  2. T
  3. F
  4. F
  5. T
  6. F

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34. Diagnosis of myasthenia gravis

  1. The titer of anti-AChR antibodies in patients with myasthenia gravis (MG) closely matches the severity of symptoms?
  2. The sensitivity of anti-AChR antibodies with pure ocular MG is between 85 – 90% ?
  3. Repetitive nerve stimulation typically shows decremental response in MG?
  4. Repetitive nerve stimulation typically shows facilitation in Lambert-Eaton myasthenic syndrome?
  5. Single-fiber electromyography is the most sensitive test for MG?
  6. Subjective improvement in muscular weakness  after intravenous edrophonium is considered as positive Tensilon test and confirmation of MG ?

  1. F
  2. F
  3. T
  4. T
  5. T
  6. F

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33. Antibodies in myasthenia gravis

  1. Antibodies against the nicotinic acetylcholine receptor (AChR) are found in 50 – 60% of patients with generalized myasthenia gravis (MG)?
  2. A majority of antibodies against the AChR found in patients with MG are “blocking” antibodies which prevent binding of acetylcholine to the AChR?
  3. Anti-AChR “binding” antibodies, bind to the AChR and cause destruction of junctional folds by activating the complement system?
  4. Most of the seronegative MG patient (those that do not have anti-AChR antibodies but have MG) have antibodies against P/Q-type VGCC (voltage gated-calcium channels)?
  5. Antibodies against LRP4, Agrin and titin proteins are shown in some seronegative MG patients ?
  6. Patients that have anti-MuSK (Muscle-Specific Kinase) antibodies suffer from Lambert–Eaton myasthenic syndrome?

  1. F
  2. F
  3. T
  4. F
  5. T
  6. F

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32. Brain tumors and grades (I)

According to “The 2016 World Health Organization Classification of Tumors of the Central Nervous System”:

  1. Pilocytic astrocytoma: WHO grade II ?
  2. Anaplastic astrocytoma: WHO grade IV ?
  3. Anaplastic oligodendroglioma: WHO grade III ?
  4. Ependymoma: WHO grade I ?
  5. Gangliocytoma: WHO grade I ?
  6. Pineoblastoma: WHO grade IV ?

  1. F
  2. F
  3. T
  4. F
  5. T
  6. T