NSSB TBL 1 - Cerebral cortex

What is the main function of the primary motor cortex?

Initiation and execution of voluntary movement via corticospinal output.

Where is the primary motor cortex located?

Precentral gyrus of the frontal lobe.

What is somatotopic organisation?

Mapping of body regions onto specific cortical areas (motor and sensory homunculus).

Which cortical area is responsible for speech production?

Broca’s area in the dominant inferior frontal gyrus.

What type of aphasia results from a Broca’s area lesion?

Nonfluent, effortful speech with impaired repetition and preserved comprehension.

Which cortical area is responsible for language comprehension?

Wernicke’s area in the dominant superior temporal gyrus.

What type of aphasia results from a Wernicke’s area lesion?

Fluent but nonsensical speech with impaired comprehension.

What is the function of the primary somatosensory cortex?

Processing of tactile, proprioceptive, and vibration sensory input.

Where is the primary somatosensory cortex located?

Postcentral gyrus of the parietal lobe.

What is the function of the auditory cortex?

Processing basic sound frequency and intensity information.

Where is the auditory cortex located?

Heschl’s gyrus in the superior temporal lobe.

What pathway carries auditory information from cochlea to cortex?

Organ of Corti → cochlear nerve → cochlear nuclei → inferior colliculus → MGN → auditory cortex.

What is the main function of the visual cortex (V1)?

Initial processing of visual input such as edges and contrast.

What is the dorsal visual stream responsible for?

Spatial awareness and motion detection (“where” pathway).

What is the ventral visual stream responsible for?

Object and face recognition (“what” pathway).

Which fibres are carried in Meyer’s loop?

Contralateral superior visual field fibres.

A lesion in right Meyer’s loop causes what deficit?

Left superior quadrantanopia.

What is the visual consequence of an optic chiasm lesion?

Bitemporal hemianopia due to nasal fibre crossing disruption.

What deficit occurs with a left optic tract lesion?

Right homonymous hemianopia.

What is macular sparing?

Preservation of central vision in occipital cortex lesions (PCA stroke).

What does the frontal eye field control?

Voluntary saccadic eye movements to the contralateral side.

What occurs with a right frontal eye field lesion?

Inability to voluntarily look left; eyes deviate toward lesion.

What is the function of the PPRF?

Horizontal gaze centre coordinating conjugate gaze.

A lesion of the PPRF causes which deficit?

Loss of ipsilateral horizontal gaze.

What is the role of the MLF?

Links abducens to oculomotor nuclei for conjugate gaze.

What clinical sign characterises internuclear ophthalmoplegia (INO)?

Impaired adduction on side of lesion with abducting nystagmus of opposite eye.

What is the role of the superior colliculus?

Reflexive orienting eye movements.

What is the function of the hippocampus?

Formation of new episodic (declarative) memories.

What is the function of the entorhinal cortex?

Gateway for cortical input to hippocampus; early site of Alzheimer’s pathology.

Which structure provides major output from the hippocampus?

The fornix.

Damage to the fornix produces what deficit?

Impaired memory consolidation and anterograde amnesia.

What structure is damaged in Korsakoff syndrome?

Mamillary bodies.

What type of memory is most affected by hippocampal lesions?

New episodic memory formation (anterograde memory).

Which type of memory is preserved in hippocampal lesions?

Procedural memory (basal ganglia and cerebellum).

What is the function of the prefrontal cortex in memory?

Working memory and executive planning.

What is the main neurotransmitter associated with attention?

Noradrenaline (locus coeruleus).

What are the three divisions of the cerebellum?

Vermis, intermediate zone, lateral hemispheres.

What is the main role of the cerebellar vermis?

Postural control and gait stability.

A lesion in the cerebellar vermis causes what?

Truncal ataxia.

What is the function of the cerebellar hemispheres?

Limb coordination and motor planning.

A lesion in the cerebellar hemispheres causes what?

Ipsilateral limb ataxia, dysmetria, intention tremor.

What is the role of the flocculonodular lobe?

Balance and eye movement coordination.

What is the hallmark of cerebellar dysfunction?

Ataxia with preserved strength.

Which nuclei are the major output of the cerebellum?

Deep cerebellar nuclei (dentate, interposed, fastigial).

What is the function of the basal ganglia direct pathway?

Facilitates voluntary movement.

What is the function of the indirect pathway?

Inhibits unwanted movement.

What is the effect of dopamine on the direct pathway?

Activates it via D1 receptors → increased movement.

What is the effect of dopamine on the indirect pathway?

Inhibits it via D2 receptors → increased movement.

What happens to basal ganglia output in Parkinson's disease?

Indirect pathway becomes overactive → excessive GPi inhibition of thalamus → hypokinesia.

What is the hallmark movement disorder of STN lesions?

Hemiballismus.

What neurotransmitter is lost in Parkinson’s disease?

Dopamine (from substantia nigra pars compacta).

What is the pathological hallmark of Parkinson’s?

Lewy bodies composed of α-synuclein.

What is the classical triad of Parkinson’s?

Resting tremor, rigidity, bradykinesia.

What is the earliest non-motor feature of Parkinson’s?

Anosmia (loss of smell).

What is Braak staging?

Pattern of ascending spread of Lewy pathology in Parkinson’s disease.

Where does Braak stage 1 pathology appear?

Olfactory bulb and dorsal motor nucleus of vagus (medulla).

At which Braak stage is the substantia nigra affected?

Stage 3.

What deficits occur when neocortex is affected in Parkinson’s?

Cognitive decline and dementia.

What is the earliest cognitive deficit in Parkinson’s disease?

Visuospatial and attention impairment.

What is the earliest cognitive deficit in Alzheimer’s disease?

Episodic memory impairment.

What proteins accumulate in Alzheimer’s disease?

Amyloid-β plaques and tau neurofibrillary tangles.

Where does Alzheimer’s pathology start?

Entorhinal cortex and hippocampus.

What is the classic triad of Lewy body dementia?

Visual hallucinations, fluctuating cognition, parkinsonism.

What distinguishes FTD from Alzheimer’s?

Early personality/behavioural changes in FTD.

What characterises vascular dementia?

Stepwise decline after multiple infarcts.

What is the hallmark EEG finding in absence seizures?

3 Hz spike-and-wave discharges.

What is the typical age of onset of childhood absence epilepsy?

4–10 years.

What is the hallmark of temporal lobe epilepsy?

Epigastric rising aura, déjà vu, automatisms.

Which lobe is associated with visual hallucinations in seizures?

Occipital lobe.

What type of seizure begins with sudden flinging limb movements?

Hemiballistic movements from STN lesion.

What is the main function of the primary visual cortex (V1)?

Simple visual processing of lines and orientation.

What deficit results from bilateral occipital lobe damage?

Cortical blindness.

What is the role of the LGN?

Relay centre for visual information from retina to visual cortex.

What role does the pulvinar play?

Visual attention and integration.

What is the major blood supply to the primary visual cortex?

Posterior cerebral artery (PCA).

What is the role of the dorsal stream in attention?

Spatial attention and visually guided action.

What is Balint syndrome?

Bilateral parietal lesions causing optic ataxia, simultagnosia, ocular apraxia.

What is prosopagnosia?

Inability to recognise faces (inferior temporal lesion).

What is the role of the SMA (supplementary motor area)?

Planning and initiation of internally generated movement.

What deficit results from SMA lesions?

Akinesia and impaired initiation of movement.

Which lobe is responsible for visuospatial processing?

Parietal lobe.

What deficit results from right parietal lobe lesions?

Left hemispatial neglect.

Which structure integrates multisensory input for attention?

Posterior parietal cortex.

Which structure is critical for fear memory?

Amygdala.

What clinical sign results from bilateral amygdala damage?

Flattened affect and loss of fear response.

Which dementia shows early language dysfunction?

Primary progressive aphasia (a variant of FTD).

Which fibres carry information from retina to optic chiasm?

Retinal ganglion cell axons (optic nerve).

Which artery supplies Broca's and Wernicke's areas?

Middle cerebral artery (MCA).

Which condition presents with intention tremor?

Cerebellar hemisphere lesions.

Which condition presents with resting tremor?

Parkinson’s disease (basal ganglia).

What is dysdiadochokinesia?

Inability to perform rapid alternating movements (cerebellar sign).

What is dysmetria?

Inaccurate targeting of movements (past-pointing).

What causes scanning speech?

Cerebellar lesions (especially hemispheric).

Which pathway mediates pupillary light reflex?

Retina → pretectal nucleus → Edinger-Westphal nucleus → oculomotor nerve.

What is the effect of a lesion in the dorsal midbrain?

Vertical gaze palsy (Parinaud syndrome).

Where is the primary auditory cortex located?

Transverse temporal gyri (Heschl’s gyrus).

What is the main role of the basal forebrain?

Cholinergic input for memory and attention.

What deficit results from basal forebrain degeneration?

Memory and attention impairment seen in Alzheimer’s disease.

Which structure links the hippocampus to mamillary bodies?

Fornix.

Which structure links mamillary bodies to thalamus?

Mammillothalamic tract.