Psychiatry and Neurology without getting lost: classification, localisation and drug links

Psychiatry and Neurology both have a way of making capable students feel lost. Psychiatry has a sprawl of named disorders that seem to blur into each other. Neurology has cranial nerves, tracts, syndromes with people's names attached, and examination findings that you only half remember from the ward. Both subjects tempt you into the same mistake: reading one disease after another until the names run together.

The way through is the same for both, even though the content is different. Impose a structure first, and hang the details on it. In psychiatry the structure is classification. In neurology it's localisation. For the drugs in both, it's the link between a drug class and the problem it treats.

A quick note on the exam itself. We don't know how the paper is currently weighted between these subjects, and patterns and counselling rules change, so look at the current NBEMS and NMC notices instead of trusting a number from anyone, including us. What follows is about learning well, whatever the weightage is.

Psychiatry: classification before content

A diagnosis in psychiatry is mostly a decision about which family the problem belongs to. If you know the families, you're already halfway to the answer in most questions. Here's a working map. Use the grouping in your own textbook, because two systems of classification (ICD and DSM) are used in teaching, and they organise things somewhat differently. Learn the one your textbook follows, and be aware of the other.

• Neurocognitive disorders: delirium and dementia.
• Substance-related disorders: alcohol, opioids, cannabis, nicotine, and the rest.
• Psychotic disorders: schizophrenia and its relatives.
• Mood disorders: depression, bipolar disorder.
• Anxiety, obsessive-compulsive and stress-related disorders: panic, phobias, OCD, post-traumatic stress, adjustment disorders.
• Somatic symptom and dissociative disorders.
• Personality disorders.
• Neurodevelopmental and childhood disorders: intellectual disability, autism spectrum, ADHD.
• Eating, sleep and sexual disorders.

Draw this map on one page. Now every disorder you read about gets a home, and the first question in any clinical vignette becomes "which family?"

The questions that choose the family

Four questions do most of the sorting.

Is the patient's consciousness or attention affected, with an acute onset? If so, think delirium, which is acute, fluctuating and usually has a medical cause. Dementia, by contrast, is gradual, with preserved alertness until late. That contrast is classic, and learning it well pays off.

Is there a loss of contact with reality? Delusions and hallucinations point to a psychotic disorder, or to a mood disorder with psychotic features, or to an organic or substance cause. Rule out the last two first.

Is the main problem mood? Persistent low mood with loss of interest, sleep and appetite changes, and guilt suggests depression. Episodes of elevated or irritable mood, with reduced need for sleep and increased activity, suggest mania, and a history of both is bipolar disorder.

Is the main problem anxiety or avoidance? Then you're in the anxiety family, and the distinguishing feature is the pattern: sudden attacks (panic), a specific trigger (phobia), intrusive thoughts and rituals (OCD), or a response following trauma (stress-related disorders).

Only after the family is decided do you reach for the specific criteria.

Schizophrenia as an example

Learn it with a frame. Symptoms are grouped as positive (hallucinations, delusions, disorganised speech), negative (blunted affect, poverty of speech, loss of motivation) and cognitive. The first-rank symptoms associated with Kurt Schneider, such as hearing voices commenting on your actions or the experience of thoughts being inserted or withdrawn, are a standard topic, so check your textbook for the list. The dopamine hypothesis explains why drugs that block dopamine D2 receptors treat positive symptoms, and why they cause side effects in the movement system. That one explanation links the disease to its drug class, which brings us to the next point.

The drug-class links in psychiatry

Psychiatric pharmacology works best as a set of short chains: class, mechanism, use, signature adverse effect.

• Typical antipsychotics: block D2 receptors. Signature problems come from that blockade in other pathways: movement disorders (acute dystonia, parkinsonism, akathisia, and later tardive dyskinesia), raised prolactin, and the rare but dangerous neuroleptic malignant syndrome.
• Atypical antipsychotics: also act on serotonin receptors, with generally fewer movement problems but more metabolic effects such as weight gain. Clozapine is the exception to remember: it is used in resistant schizophrenia, and it can cause agranulocytosis, so blood counts are monitored.
• Lithium: a mood stabiliser with a narrow therapeutic range. Learn tremor, polyuria from nephrogenic diabetes insipidus, hypothyroidism, and the need to check levels.
• SSRIs: raise serotonin at the synapse, and are first-line in depression and many anxiety disorders. Typical problems are gastrointestinal upset, sexual dysfunction, and, in overdose or with interacting drugs, serotonin syndrome.
• Tricyclic antidepressants: older, with anticholinergic effects and danger in overdose because of effects on the heart.
• MAO inhibitors: a food interaction with tyramine can produce a hypertensive crisis.
• Benzodiazepines: enhance GABA-A activity. Sedation, dependence and respiratory depression in overdose. Flumazenil reverses them.

Notice how the adverse effects follow from the mechanism. Drugs that block dopamine cause movement problems because dopamine controls movement. Drugs with anticholinergic action cause dry mouth, constipation and blurred vision for the same reason atropine does. When you understand why, you rarely need to memorise.

Alcohol deserves its own page, since it links psychiatry, medicine and neurology. Learn the sequence of withdrawal (tremor, then possible seizures, then delirium tremens) and the reason thiamine is given before glucose to people at risk: to prevent or treat Wernicke's encephalopathy. Know that disulfiram works by blocking acetaldehyde breakdown.

Neurology: localisation is the whole game

If psychiatry is classification, neurology is localisation, and the logic is simple enough to carry in your head. Given a set of signs, you ask where in the nervous system a single lesion could explain them. Then you ask what kind of lesion it is.

Step one: upper or lower motor neuron

This is the first fork in any weakness question.

• Upper motor neuron lesion: weakness with increased tone (spasticity), brisk reflexes, an upgoing plantar response, and little wasting.
• Lower motor neuron lesion: weakness with reduced tone (flaccidity), reduced or absent reflexes, visible wasting, and sometimes fasciculations.

Everything else in motor neurology hangs off this contrast.

Step two: walk up the pathway

Now place the lesion along the route, from muscle up to cortex.

• Muscle and neuromuscular junction: weakness without sensory loss. Myasthenia gravis gives fatigable weakness that worsens with use, including drooping eyelids and double vision, and involves antibodies to the acetylcholine receptor.
• Peripheral nerve and root: sensory and motor signs that follow a nerve or a root. Guillain-Barré syndrome gives an ascending, symmetrical weakness with loss of reflexes, classically with raised CSF protein and a normal cell count.
• Spinal cord: a sensory level, with weakness and altered tone below it. In a hemisection (Brown-Séquard syndrome), the same side loses motor function and position sense below the lesion, and the opposite side loses pain and temperature. Learn why, by tracing where each tract crosses.
• Brainstem: look for crossed signs, meaning cranial nerve signs on one side and limb signs on the other, because the cranial nerve nuclei sit at the level of the lesion and the long tracts cross lower down.
• Cerebellum: ataxia, intention tremor, nystagmus and difficulty with rapid alternating movements. Cerebellar hemisphere lesions cause signs on the same side as the lesion.
• Basal ganglia: movement disorders. Parkinson's disease is the loss of dopaminergic neurons in the substantia nigra, with resting tremor, rigidity and slowness, and it is treated with levodopa, which links to pharmacology. Huntington's disease is a trinucleotide repeat disorder with chorea.
• Internal capsule and cortex: a capsular lesion can cause a dense hemiparesis, whereas cortical lesions produce specific deficits such as aphasia or neglect.

Step three: stroke syndromes by vessel

Vascular territories are a standard exam area, and one table covers them. A middle cerebral artery stroke typically gives weakness and sensory loss of the opposite face and arm more than the leg, with aphasia if the dominant hemisphere is involved. An anterior cerebral artery stroke affects the opposite leg more than the arm. A posterior cerebral artery stroke gives visual field loss. A lateral medullary syndrome (Wallenberg), from a posterior inferior cerebellar artery or vertebral occlusion, gives a pattern of crossed sensory loss with other brainstem features, and it is a good test of your tract anatomy. Check the exact features in your textbook before relying on this sketch.

Step four: the type of lesion

Once localised, consider the time course. Sudden onset suggests a vascular event. Subacute progression suggests tumour, infection or inflammation. Relapsing and remitting with different sites points to demyelination, as in multiple sclerosis. Gradual progression over years points to a degenerative process. Meningitis is a useful CSF exercise: bacterial typically shows neutrophils, high protein and low glucose; viral typically shows lymphocytes with normal glucose; tuberculous typically shows lymphocytes with high protein and low glucose. Verify the numbers in your textbook, but remember the pattern.

Epilepsy and its drug links

Classify seizures first into focal and generalised, then link each to the drugs. Valproate has a broad spectrum. Carbamazepine is used for focal seizures and is not suitable for absence seizures, which are treated with agents such as ethosuximide or valproate. Phenytoin is used in focal and generalised tonic-clonic seizures and has the narrow therapeutic range and gum changes you already know from pharmacology. Drug choices and guidance are revised from time to time, and certain agents carry special risks in pregnancy, so check a current textbook before assuming a first-line choice.

Where the two subjects meet

Psychiatry and neurology overlap more than the syllabus suggests, and the overlaps are exam-friendly. Delirium and dementia belong in both. Learn the dementias by their signature: Alzheimer's with early memory loss, vascular dementia with a stepwise course, dementia with Lewy bodies with visual hallucinations, fluctuating cognition and parkinsonism, and frontotemporal dementia with early change in behaviour. Wernicke's and Korsakoff's link alcohol, thiamine and memory. Seizures can have psychiatric presentations, and some psychiatric drugs lower the seizure threshold. A question that looks like psychiatry may be testing neurology, and the reverse.

How to practise

Both subjects reward practice with short clinical vignettes more than rereading. When you attempt a neurology question, say your localisation out loud before you look at the options: "upper motor neuron, right side, with a left facial nerve sign, so brainstem". When you attempt a psychiatry question, name the family first. If you want a place to try this, our practice questions give an explanation for each option, though they are original practice material and not exam questions, so cross-check anything important with your textbook.

Keep a single sheet per subject: the psychiatric family map with one defining feature each, and a neurology flowchart of the four localisation steps. Redraw it from memory every week.

What to do this week

1. Draw the psychiatric family map from memory, add one defining feature to each family, and fix gaps from your textbook.
2. Write the delirium versus dementia contrast and the upper versus lower motor neuron contrast on one card each.
3. Make a drug-class table for psychiatry with four columns: class, mechanism, use and signature adverse effect.
4. Practise localising: take five neurology vignettes from your textbook or notes and name the lesion site before reading the answer.
5. Trace the spinal tracts for pain and temperature, and for position sense, then explain Brown-Séquard syndrome aloud to a friend or to yourself.