Neurology Practice Tests with Answers: 50 Questions for Exam Preparation

The spinal tract of the trigeminal nerve and its nucleus form a characteristic elevation on the dorsolateral surface of the medulla oblongata — the tuberculum cinereum.

The posterior roots of the spinal cord are formed by axons of sensory (pseudounipolar) neurons of the spinal ganglia, which conduct afferent impulses from peripheral receptors to central nervous system structures.

Nuclear bag fibers in muscle spindles respond to rapid changes in muscle length (dynamic response), whereas nuclear chain fibers register its constant length.

The branches of the vertebral artery supplying the spinal cord form a single network with the radicular branches of the segmental arteries of the neck, trunk, and deep cervical arteries. This ensures reliable collateral circulation at different levels of the spinal cord.

A bilateral lesion of the medial-rostral parts of the dorsomedial thalamus disrupts the functions of the reticular formation and limbic connections, leading to disorders of consciousness (hypersomnia, apathy) and severe amnesia.

Traditionally, the description of the Papez circuit begins with the hippocampus, from which nerve impulses travel via the fornix to the mammillary bodies of the hypothalamus.

The cortical representation of facial sensation is located in the lower third of the postcentral gyrus. Because the sensory pathways decussate, sensory impairment on the right half of the face results from a lesion in the left hemisphere.

The main (pontine) sensory nucleus of the trigeminal nerve, responsible for tactile and proprioceptive sensation of the face, is located in the tegmentum of the pons.

Fibers of the deep sensation pathways from the upper extremities travel within the cuneate fasciculus and synapse on second-order neurons in the ipsilateral nucleus cuneatus of the medulla oblongata. The gracile fasciculus carries analogous information from the lower extremities.

Axons of neurons from the gracile and cuneate nuclei decussate at the level of the medulla oblongata (forming the internal arcuate fibers) and form the medial lemniscus, which conducts deep sensation.

The nucleus of the spinal tract of the trigeminal nerve (nucleus tractus spinalis nervi trigemini) provides pain and temperature sensation for the face.

Astereognosis occurs with lesions of the secondary somatosensory areas of the cortex located in the superior parietal lobule posterior to the postcentral gyrus. Because the sensory pathways decussate, symptoms develop on the side contralateral to the lesion.

The stapedial nerve is a branch of the facial nerve and provides motor innervation to the corresponding muscle (m. stapedius) within the tympanic cavity.

When the facial nerve trunk itself or its nucleus is damaged, the innervation of the entire half of the face on the side of the lesion is impaired, which manifests as weakness of both the upper and lower facial expression muscles.

The motor nucleus of the facial nerve innervating the upper face receives bilateral cortical innervation; therefore, in unilateral cortical lesions, only the lower half of the facial musculature on the opposite side is affected.

The superior salivatory nucleus is a parasympathetic nucleus of the intermediate (facial) nerve. It lies in the tegmentum of the pons in close proximity to the motor nucleus of the facial nerve.

A lesion of the nucleus or trunk of the facial nerve results in peripheral paralysis involving all muscles of one half of the face, both in the upper and lower tiers.

The upper part of the facial nerve nucleus receives bilateral cortical innervation, whereas the lower part receives only contralateral innervation; therefore, in central paresis, only the lower half of the face on the side opposite to the lesion is affected.

The hypoglossal nerve innervates the muscles of the tongue, so its lesion impairs tongue mobility, which clinically manifests as a speech articulation disorder (dysarthria).

In unilateral lesion of the hypoglossal nerve or its nucleus, the tongue deviates towards the weak muscle upon protrusion, i.e., towards the lesion in peripheral paresis.

A lesion of the hypoglossal motor nucleus causes peripheral paralysis accompanied by denervation changes directly in the muscle tissue of the tongue — atrophy and fascicular twitching.

The motor nucleus of the hypoglossal nerve lies in the medulla oblongata in the region of the hypoglossal trigone. This area is located in the lower part of the rhomboid fossa, which forms the floor of the IV ventricle.

In peripheral lesions of the hypoglossal nerve, the healthy genioglossus muscle pushes the tongue toward the weak (affected) side.

A lesion of the hypoglossal motor nucleus causes peripheral paralysis of the tongue muscles. Nuclear lesions, in addition to weakness and atrophy, are characterized by the appearance of fasciculations — spontaneous contractions of individual muscle bundles.

In infants, the cranial sutures are not yet fused, so elevated intracranial pressure in hydrocephalus is compensated by separation of the sutures and a visible increase in head size.

The bulk of cerebrospinal fluid is resorbed into the venous system through arachnoid granulations (Pachchioni granulations) protruding into the lumen of the dural venous sinuses.

Non-communicating hydrocephalus occurs when there is a mechanical obstruction to CSF flow within the ventricular system or at its outflow, prior to the fluid reaching the subarachnoid space for absorption.

Cerebrospinal fluid drains from the fourth ventricle into the cranial and spinal subarachnoid space through three openings: the unpaired median aperture (foramen of Magendie) and the two lateral apertures (foramina of Luschka).

The bulk of cerebrospinal fluid is reabsorbed into the venous system via arachnoid granulations (Pachchioni granulations) projecting into the lumen of the dural venous sinuses.

According to clinical guidelines, patients with ischemic stroke who have not undergone thrombolytic therapy are prescribed acetylsalicylic acid at a dose of 150–300 mg/day within the first 24–48 hours.

Systemic intravenous thrombolysis is the pharmacological dissolution of a thrombus using recombinant tissue plasminogen activator administration.

The anterior cerebral artery supplies the medial regions of the frontal and parietal lobes, including the paracentral lobule, which houses the cortical centers for voluntary motor function and sensation of the contralateral lower extremity.

In its proximal segment, the middle cerebral artery gives off the lateral and medial lenticulostriate arteries, which supply the internal capsule and basal ganglia.

Focal (partial) seizures occur due to a local epileptiform discharge in a limited area of the cerebral cortex of one hemisphere.

The classical electroencephalographic pattern of typical absence seizures is generalized symmetrical 3 Hz spike-and-slow-wave discharges.

In elderly patients (over 60 years old), the most frequent cause of newly onset epileptic seizures is cerebrovascular disease, such as previous strokes or chronic cerebral ischemia.

If a high (therapeutic) blood concentration of an antiepileptic drug is achieved while seizures persist, this indicates that the drug is ineffective. In such situations, switching to another medication is required rather than further increasing the dose.

Simple and complex partial seizures acting as an aura before generalized convulsive seizures include sensory, autonomic, motor, and psychic phenomena.

In trigeminal neuralgia, intense pain is often accompanied by a reflex spasm of the facial muscles on the affected side, historically termed "tic douloureux".

For pharmacoresistant trigeminal neuralgia when neurosurgical treatment is not feasible, current clinical guidelines indicate local injections of botulinum toxin type A.

The pathogenesis of trigeminal neuralgia involves hyperactivation of structures within the facial nociceptive system: impulses are conducted from the trigeminal nuclei in the brainstem to the thalamus and further to the somatosensory cortex, generating the pain syndrome.

Classical (idiopathic) trigeminal neuralgia is most commonly caused by neurovascular conflict. Pain attacks occur due to compression of the nerve root by a blood vessel loop at the zone of its exit from the pons.

The bilateral nature of pain and the persistent interictal algic component are atypical for classical idiopathic neuralgia, but are frequently observed in demyelinating diseases of the CNS.

The optic tract is a retrochiasmal structure containing fibers from the outer half of the ipsilateral retina and the inner half of the contralateral retina. Its unilateral damage leads to the loss of opposite visual fields in both eyes (homonymous hemianopia).

In the region of the optic chiasm, crossing fibers from the nasal halves of the retinas are damaged, which collect information from the temporal visual fields of both eyes.

In the optic chiasm region, fibers from the inner (nasal) halves of the retinas cross; therefore, when it is damaged, the outer (temporal) visual fields are lost on both sides.

Bitemporal hemianopia occurs when the medial part of the optic chiasm is damaged, where crossing nerve fibers from the nasal halves of the retinas of both eyes pass. These fibers are responsible for perceiving the outer (temporal) visual fields.

The primary visual cortex performs only basic signal processing, whereas the synthesis, pattern recognition, and conscious awareness of visual information occur in the secondary (associative) visual areas.

Tuberculous meningitis is characterized by a subacute, granulomatous nature of inflammation with a gradual increase in symptoms over several weeks, unlike the acute course of viral meningitides.

Migrating annular erythema at the tick bite site is a pathognomonic early clinical marker of Ixodes borreliosis. The other listed symptoms are characteristic of spinal cord damage (myelitis).