A 35-year-old male smoker with complaints of difficulty in swallowing and ulcer on tip of his tongue for last one month, visits…

(a)(i) Lymphatic spread of carcinoma of the tongue tip

The tip drains to the submental nodes, bilaterally, and also directly to the deep cervical chain. The principal node of the tongue is the jugulo-omohyoid node, where the tongue's lymph finally collects.

Flow of spread: tip of tongue → submental nodes (Level IA) → submandibular nodes (Level IB) → upper deep cervical nodes, including the jugulodigastric node (Level II) → jugulo-omohyoid node, the principal node (Level III) → lower deep cervical nodes (Level IV) → jugular lymph trunk → thoracic duct on the left or right lymphatic duct on the right → junction of the internal jugular and subclavian veins.

The lateral border drains to submandibular and upper deep cervical nodes, and the posterior part to the jugulodigastric node. Because the tip and midline drain bilaterally, contralateral neck metastases occur, so levels I to V are assessed in staging and neck dissection.

(a)(ii) Role of the tongue in swallowing

In the oral phase (voluntary), the tongue forms the food into a bolus, lifts against the hard palate and squeezes the bolus backwards in a front-to-back wave. In the pharyngeal phase (involuntary), the base of the tongue retracts to push the bolus into the pharynx while the soft palate seals the nasopharynx, the larynx rises and the epiglottis covers the airway. The tongue also gives taste and touch feedback that triggers the reflex. In this patient, a lesion with poor mobility makes bolus control and propulsion difficult, causing dysphagia and a risk of aspiration.

(b)(i) Course of the auditory pathway

Sound vibrations pass through the tympanic membrane, ossicles and oval window to the cochlear fluid, which moves the basilar membrane and bends the hair cells of the organ of Corti.

1. First-order neurons are the bipolar cells of the spiral ganglion; their fibres form the cochlear nerve.
2. The cochlear nerve ends in the dorsal and ventral cochlear nuclei at the pontomedullary junction.
3. Second-order fibres cross through the trapezoid body to the superior olivary nuclei, mostly of the opposite side; some stay uncrossed. Sound localisation begins here.
4. Fibres ascend in the lateral lemniscus to the inferior colliculus of the midbrain.
5. The inferior colliculus projects through the brachium to the medial geniculate body of the thalamus.
6. The auditory radiation passes through the sublenticular part of the internal capsule to the primary auditory cortex (areas 41 and 42, Heschl's gyrus in the superior temporal gyrus).

Because of the crossing and the ipsilateral fibres, each cortex receives input from both ears.

(b)(ii) Blood supply of the auditory cortex

The auditory cortex on the superior temporal gyrus is supplied by the temporal branches of the middle cerebral artery, mainly its inferior division, with a small contribution from the posterior cerebral artery on the inferior temporal surface. The auditory radiation in the internal capsule is supplied by lenticulostriate and anterior choroidal branches, and the medial geniculate body by the posterior cerebral artery. Since each cortex hears from both ears, a unilateral infarct causes only mild hearing loss; bilateral lesions cause cortical deafness.

(c) Folic acid: sources, RDA, deficiency and folate trap

Sources: green leafy vegetables (spinach, amaranth, fenugreek), pulses such as chana and moong, liver, yeast, groundnuts, citrus fruits and fortified cereals. Folate is destroyed by prolonged cooking. ICMR-NIN 2020 RDA: 300 μg/day for adult men, 220 μg/day for adult women, 570 μg/day in pregnancy and 330 μg/day in lactation.

Deficiency impairs thymidylate and purine synthesis, so DNA synthesis falls in rapidly dividing cells. Clinical effects are megaloblastic anaemia with macro-ovalocytes and hypersegmented neutrophils, glossitis, diarrhoea from mucosal atrophy, and sometimes pancytopenia. Maternal deficiency causes neural tube defects, and raised homocysteine adds to vascular risk. Unlike vitamin B12 deficiency, there are no neurological deficits.

Folate trap. Folate enters the cell as N⁵-methyl-tetrahydrofolate (N⁵-methyl-THF). Its only route back to THF is through methionine synthase, which transfers the methyl group to homocysteine and needs vitamin B12. In B12 deficiency this step stops and the methylation of N⁵,N¹⁰-methylene-THF to N⁵-methyl-THF is irreversible, so folate accumulates as N⁵-methyl-THF and the free THF pool falls. Cells then behave as if folate-deficient, with megaloblastic anaemia, although serum folate is normal or high. Folic acid corrects the anaemia but not the neuropathy, so it can mask B12 deficiency.

(d) Role of the cerebellum in voluntary movement and cerebellar dysfunction

The cerebellum does not start movement. It smooths and coordinates it by comparing the intended movement from the cortex with the actual movement reported by proprioceptors, and sending correcting signals. The vestibulocerebellum (flocculonodular lobe) controls balance, posture and eye movements through the vestibular nuclei. The spinocerebellum (vermis and paravermis) receives spinocerebellar input, regulates muscle tone, and corrects ongoing limb and trunk movements. The cerebrocerebellum (lateral hemisphere) plans and times voluntary movement through the pontocerebellar input and the dentate–thalamic–motor cortex loop, and stores learned motor skills. The cerebellum acts on the cortex through the thalamus, so a lesion produces clumsiness, not paralysis.

Dysfunction gives ipsilateral signs: ataxic gait with a wide base, intention tremor, dysmetria (past-pointing), dysdiadochokinesia, rebound phenomenon, hypotonia, pendular reflexes, nystagmus and scanning speech. Vermis lesions cause truncal ataxia, and hemisphere lesions cause limb ataxia.

(e) Genesis of REM sleep and why it is paradoxical

REM sleep is generated in the pons. REM-on neurons in the pontine reticular formation, including cholinergic cells of the pedunculopontine and laterodorsal tegmental nuclei and the sublaterodorsal nucleus, fire and activate the thalamus and cortex. They produce ponto-geniculo-occipital (PGO) waves and rapid eye movements. At the same time the REM-off monoaminergic cells, the noradrenergic locus coeruleus and serotonergic raphe nuclei, fall silent, and the sublaterodorsal nucleus activates inhibitory medullary neurons that hyperpolarise spinal motor neurons, producing muscle atonia. The cycle recurs about every 90 minutes and takes up 20 to 25% of adult sleep.

It is called paradoxical sleep because the EEG shows low-voltage, fast, desynchronised activity like wakefulness, and the brain is highly active with vivid dreams and irregular autonomic activity, yet the skeletal muscles are paralysed (except the extraocular and respiratory muscles) and the arousal threshold is raised.