Speech and Higher Mental Function Examination Viva

Short Case Viva Defence — Case A: Acute Wernicke Aphasia

Candidate's opening statement (model answer)

"I examined Mrs Kaur, a 72-year-old woman, brought in forty minutes after the sudden onset of strange speech. She is alert and afebrile. On examination of the speech, spontaneous speech is fluent — long phrases, normal melody, effortless — but the content is empty, with frequent phonemic and verbal paraphasias and several neologisms. She does not appear frustrated by her speech. Comprehension is impaired: she manages an occasional one-step command but cannot follow a two-step command. Repetition is impaired — she cannot repeat 'no ifs, ands, or buts.' Naming is impaired for a watch, a pen and the fingers. Hearing is intact to a whispered number in each ear, so this is not a peripheral auditory problem. Attention, tested by digit span and months backwards, is preserved. [1]

'In summary, this patient has a fluent aphasia with impaired comprehension and impaired repetition — a Wernicke aphasia. The sudden onset in a vasculopathic patient localises to the dominant superior temporal gyrus in the inferior division of the left middle cerebral artery, and this is an acute stroke. The emergency registrar has labelled her confused, but her preserved alertness and attention, her focal language-specific deficit, and the discrete sudden onset confirm a focal aphasia, not delirium. My immediate priority is to activate the acute stroke pathway for urgent CT to exclude haemorrhage, then assess for thrombolysis and thrombectomy.'" [1]

Examiner probing questions and model answers

Q1: "How do you know this is aphasia and not delirium?" [1]

"Because the core features of delirium are absent. Delirium is defined by an acute, fluctuating impairment of attention with altered consciousness, and this patient has preserved alertness and attention — she is fully awake, she manages one-step commands, and her digit span is preserved. In delirium the speech is globally disorganised — rambling, tangential, off the point — whereas here the fluency and melody are normal and only the content is disordered, with specific language errors: phonemic paraphasias, verbal paraphasias and neologisms. Those are language errors of a focal type, not the jumbled thinking of an acute confusional state. The onset is sudden and discrete, consistent with a vascular event, rather than the fluctuating, precipitant-driven course of delirium. The danger of the confusion label is that a patient with an acute dominant-hemisphere stroke is worked up for sepsis while the thrombolysis clock runs out, so I would confirm attention formally with digit span and months backwards, and then activate the stroke pathway." [1]

Q2: "Walk me through your classification of this aphasia." [1]

"I classify on three axes — fluency, comprehension and repetition — because no single axis is sufficient. First, fluency: she speaks in long phrases with normal melody and rate, so she is fluent. That puts the lesion posteriorly, in the temporal or parietal language area rather than the frontal Broca area. Second, comprehension: she cannot follow a two-step command, so comprehension is impaired. A fluent aphasia with impaired comprehension narrows it to Wernicke or transcortical sensory. Third, repetition: she cannot repeat 'no ifs, ands, or buts,' so repetition is impaired. That distinguishes Wernicke from transcortical sensory, because the transcortical aphasias — by definition — preserve repetition. So fluent plus impaired comprehension plus impaired repetition is Wernicke aphasia, from a left superior temporal gyrus lesion. The preserved repetition of a transcortical aphasia tells me the perisylvian language loop is intact and the lesion is in the watershed territory; the impaired repetition here tells me the perisylvian cortex itself is involved, which is the MCA territory." [1]

Q3: "What is your evidence base for speech therapy once she stabilises?" [1]

"The Brady 2016 Cochrane review of speech and language therapy for aphasia following stroke, which pooled 57 randomised trials and about 3000 participants. It found that speech and language therapy improves functional communication, receptive language and expressive language compared with no therapy, with a suggestion that higher intensity and dose are more effective [4]. It did not find enough evidence to favour one therapeutic approach over another, or to settle group versus individual therapy. So the practical position is to refer early to a speech and language therapist, deliver therapy at a clinically meaningful intensity — not a token weekly session — and set functional communication goals. I would also involve the family in supported communication strategies from the outset, because the social impact of aphasia is substantial and is often under-recognised."

Short Case Viva Defence — Case B: Conduction Aphasia

Candidate's opening statement (model answer)

"I examined Mr Hadid, a 60-year-old man, assessed three days after a left-hemisphere stroke. He speaks in fluent, grammatical sentences and conveys meaning, and he understands both one-step and two-step commands. However, when I ask him to repeat 'no ifs, ands, or buts,' he produces 'no ifs, ants, or buts,' and on a second attempt 'no ifs, ands, or cuts,' visibly struggling. His repetition is noticeably worse than his spontaneous speech. Naming is mildly impaired. He is frustrated by the repetition task, which he performs far worse than his conversation. [1]

'In summary, this is a fluent aphasia with preserved comprehension but severely impaired repetition — a conduction aphasia. The paradox that he can speak and understand but cannot echo what he has just heard localises to the arcuate fasciculus, the white-matter bundle that carries the decoded word from Wernicke area to Broca area for re-articulation. The lesion is usually a left superior temporal or supramarginal gyrus infarct. Repetition is the most localising of the language axes because it tests a single tract.'" [1]

Examiner: "Why can he speak and understand but not repeat?" [1]

"Because the language input and the language output are intact, but the bridge between them is severed. Wernicke area, in the superior temporal gyrus, decodes the heard word into its meaning — and that is intact, which is why his comprehension is preserved. Broca area, in the inferior frontal gyrus, assembles the motor programme to speak the word — and that is intact, which is why his spontaneous speech is fluent and grammatical. The arcuate fasciculus is the white-matter bundle that carries the decoded auditory word from Wernicke area forward to Broca area so it can be re-articulated. When that bundle is damaged — classically by a left temporoparietal infarct — the patient can generate their own words and understand yours, but they cannot take your words and pass them through the system to repeat them. So repetition fails while fluency and comprehension survive. It is the cleanest demonstration in clinical neurology that a white-matter tract, not a cortical area, can be the sole seat of a deficit." [1]

Examiner: "How does this differ from the transcortical aphasias, where repetition is preserved?" [1]

"The transcortical aphasias are the mirror image of conduction aphasia. In a transcortical aphasia, the perisylvian language cortex — Broca, Wernicke and the arcuate fasciculus — is preserved as an intact, self-contained circuit. The lesion is in the watershed territory around it, which disconnects the language area from the rest of the brain but leaves the internal circuitry intact. Because the circuit is intact, the patient can echo — repetition is preserved, often strikingly so, even for long sentences they could never generate themselves. But because the area is disconnected from the rest of the brain, they cannot create spontaneous speech (transcortical motor) or cannot comprehend it (transcortical sensory), or both (mixed transcortical). So preserved repetition is the signature of a watershed-territory lesion, and impaired repetition is the signature of a perisylvian (MCA-territory) lesion. In conduction aphasia, the lesion is within the perisylvian loop, in the fasciculus itself, so repetition is impaired even though the cortical areas at each end are spared." [1]

Short Case Viva Defence — Case C: Progressive Cognitive Domain Profile

Candidate's opening statement (model answer)

"I examined Mr Lindqvist, a 69-year-old man, referred to the memory clinic with 18 months of progressive forgetfulness reported by his wife. He is alert and attentive, with a digit span of six forward and four backward. Immediate registration of three objects is intact, but at three minutes he recalls none of them, and cueing does not help him. He names objects and follows commands fluently and correctly. His clock drawing is normal, and he copies the intersecting pentagons accurately. On the ACE-III he scores 76 out of 100, with a memory domain of 8 out of 20 and the other domains — attention, fluency, language and visuospatial — relatively preserved between 16 and 18. [1]

'In summary, this patient has a progressive cognitive decline with a memory-dominant domain profile and relative sparing of language, visuospatial and executive function. This is the classical signature of Alzheimer disease, in which the earliest pathology in the entorhinal cortex and hippocampus produces an episodic memory deficit that does not benefit from cueing, while the neocortical functions are preserved until later. My next steps are a collateral history from his wife, formal neuropsychology, an MRI brain to look for hippocampal atrophy and exclude other causes, and a reversible-cause screen including mood, B12, thyroid and folate.'" [1]

Examiner: "How would a different domain profile change your differential?" [1]

"The domain profile is the single most useful piece of information in a cognitive workup, because each dementia subtype has a signature early deficit. A memory-dominant profile with cueing-insensitive recall, as in this patient, points to Alzheimer disease. A fluency- or language-dominant profile — a progressive non-fluent aphasia with effortful halting speech, or a semantic dementia with loss of word meaning and surface dyslexia — points to frontotemporal dementia, in which memory is relatively spared early. An attention- and processing-speed-dominant profile with slowed thinking and executive dysfunction, often on a background of vascular risk factors and with white-matter change on imaging, points to vascular cognitive impairment. A profile dominated by visuospatial impairment, fluctuating attention and visual hallucinations points to dementia with Lewy bodies. A profile of relatively preserved memory with striking behavioural and personality change — disinhibition, apathy, loss of empathy — points to the behavioural variant of frontotemporal dementia. So the domain profile does not just quantify severity; it frames the subtype and the prognosis." [1]

Examiner: "Why the ACE-III rather than the MMSE here?" [1]

"Because the question in a memory clinic is 'which dementia subtype?', and that requires a domain profile, which the ACE-III provides and the MMSE does not [3]. The MMSE returns a single 30-point score weighted toward language and orientation; it is a useful ward orientation screen but it is insensitive to mild cognitive impairment and it masks the domain pattern [1]. The ACE-III is a 100-point test scored across five domains — attention, memory, fluency, language and visuospatial — so it gives the pattern-of-deficit analysis that discriminates the subtypes. The MoCA is more sensitive than the MMSE to mild impairment and is the right choice for a quick screen in a stroke or Parkinson clinic, but it does not give the same five-domain resolution as the ACE-III [2]. So for a structured memory-clinic assessment where I am trying to distinguish Alzheimer disease from frontotemporal dementia from a vascular cognitive impairment, the ACE-III is the correct instrument. None of these screens is diagnostic — all are triggers for formal neuropsychology and imaging — but the ACE-III gives me the map I need."