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Lobes of brain

Paracentral lobule

  1. Para central lobule is formed by the medial extension of the precentral and post central gyri.
  2. It is supplied by branches of the anterior cerebral artery
  3. Neurons in paracentral lobule are concerned with:
    1. Motor and Sensory innervations of the contralateral lower extremity
    2. Regulation of physiological function such as defecation and micturition
  4. Damage of paracentral lobule occurs from occlusion of anterior cerebral artery
  5. Characteristic manifestation include
    1. Contralateral lower limb muscle weakness           
    2. Urinary incontinence
  1. Frontal lobe
    Frontal lobe lesion
    1. Foster Kennedy syndromeQ
      Features: Ipsilateral optic atrophy and contralateral papilledema
    2. A tumor of the frontal lobe is likely to damage the pre-frontal network. This presents as two relatively distinct syndromes.
      1. Frontal disinhibition syndrome
        1. Socially disinhibited and shows severe impairment of judgment, insight and foresight.
        2. Antisocial behaviour is a characteristic feature of frontal disinhibition syndrome produced from frontal lobe damage
      2. Frontal abulic syndrome
        1. Loss of initiative, creativity and curiosity
        2. Pervasive emotional apathy and blandness
        3. Akinetic mutism 
    3. Urinary incontinence can occur in lesion of paracentral lobule area of frontal lobe.
    4. Frontal release signs – Grasp reflex, palmomental response, rooting reflex.

Extra Edge:
1. Urinary incontinence is a feature of frontal lobe lesion.
2. Akinetic mutism is a term describing patients tending neither to move (akinesia) nor speak (mutism). It is the result of severe frontal lobe (LQ 2012) injury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.

  1. Parietal lobe
    Cortical function (Parietal lobe)
    1. Two point discrimination
    2. Stereognosis
    3. Graphesthesia
    4. Touch localization (Bilateral simultaneous stimulation.)  

Features of parietal lobe lesions

  1. Unilateral Parietal Lobe
    1. Contralateral hemisensory loss                              
    2. Astereognosis
    3. Agraphesthesia                                                               
    4. Contralateral homonymous Lower quadrantanopia
    5. Asymmetry of optokinetic Nystagmus (OKN)       
    6. Sensory Seizures
    7. Extinction phenomenon (contralateral)
  2. Dominant Hemisphere
    1. Dysphasia/Aphasia
    2. Dyscalculia
    3. Dyslexia
    4. Apraxia
    5. Agnosia (Tactile Agnosia)
    6. Gerstmann Syndrome
  3. Non Dominant Hemisphere
    1. Spatial disorientation
    2. Constructional apraxia
    3. Dressing apraxia
    4. Anosognosia

Extra Edge:

  1. Anosognosia is a condition in which a person who suffers disability seems unaware of the existence of his or her disability.
  2. Dyslexia is a learning disability that impairs a person's fluency or comprehension accuracy in being able to read.
  3. Astereognosis - Inability to determine 3-D shape by touch.       
  4. Agraphaesthesia – Inability to ‘read’ numbers or letters drawn on hand, with eyes shut.
  5. Apraxia – Inability to perform complex movements in the presence of normal motor, sensory and cerebellar function.
  6. Agnosia – Inability to recognize or discriminate.

Extra Edge: Gerstmann syndrome (Dominant parietal lobe disease (Ref. Hari. 18th ed., Pg- 206)



  1. Acalculia
  2. Agraphia
  3. Finger anomia
  4. Difficulty in differentiation of right and left.

Extra Edge: Aphasia, Acalculia are features of dominant (left) parietal lobe lesion.


Extra Edge: Hemineglect or neglect of contralateral side is a feature of either of Parietal lobe lesion.
(Ref. Hari. 18th ed. Pg- 207)

  1. Temporal lobe

Features of Temporal lobe lesions

  1. Unilateral Temporal Lesion
    1. Contralateral homonymous upper quadrantanopia (Sector Anopsia)
    2. Complex hallucinations (Smell, sound, vision, memory)
  1. Dominant Hemisphere
    1. Receptive aphasia
      1. Wernicke's Aphasia
      2. Anomic Aphasia
    2. Dyslexia
    3. Impaired verbal memory
    4. Word Agnosia, Word deafness
  1. Non Dominant Hemisphere
    1. Impaired non-verbal memory
    2. Impaired musical skills
    3. Prosopagnosia
  1. Bitemporal lesions (Additional Features)
    1. Deafness
    2. Apathy (Affective in difference)
    3. Impaired learning and Memory
    4. Amnesia, Korsakoff syndrome, Kluver Bucy syndrome

Extra Edge: Prosopagnosia is a disorder of face perception where the ability to recognize faces is impaired, while the ability to recognize other objects may be relatively intact.


Extra Edge:


Bilateral anterior temporal lobe involvement including amygdala- Kluver Bucy syndrome
Features: Apathy with excess sexual drive, hyperphagia, hyper-orality, visual agnosia, docility, hyper-metamorphopsia, antegrade amnesia.     


Lesions of medial temporal lobe

Unilateral lesion affecting dominant lobe (left)

Unilateral lesion affecting Non dominant lobe (right)

Bilateral lobe involvement

Verbal memory loss (Auditory Amnesia)

Non Verbal memory loss (e.g Visual Amnesia)

Antegrade Amnesia

Loss of new learning an recent memory


mportant Point:

Wernicke's Aphasia, contralateral superior homonymous quadrantopia, auditory & visual hallucinations are all features of temporal lobe lesions.

Important Point:

Medial temporal lobe and hippocampal gyrus involvement may cause an acute disturbance in memory particularly if it occurs in the dominant hemisphere.

Important Points: about visual pathway.


a. Source

b. Path

c. Information

d. Damage

i. Fibers from the inferior retina (also called "Meyer's loop"

i. Pass through the temporal lobe 

i. Carry information from the superior part of the visual field

i. A lesion in the temporal lobe that results in damage to Meyer's loop causes a characteristic loss of vision in a superior quadrant (quadrantanopia.)

ii. Fibers from the superior retina (also called "Baum's loop")

ii. Travel straight back through the parietal lobe 

ii. Carry information from the inferior part of the visual field

ii. A lesion in the parietal lobe that results in damage to Baum’s loop causes a characteristic loss of vision in a inferior quadrant (quadrantanopia.)

  1. Occipital lobe:
    Disease: Cortical blindness Q
    Features: Patient has no problem in both the Eyes but he cannot see.





Fig: Mechanisms of speech and language.

Anatomy & Physiology

  1. The primary auditory cortex is a region of the brain that processes sound and thereby contributes to our ability to hear.
  2. Broca’s area = Lies in dominant inferior frontal gyrus (LQ 2012). It is motor speech area.
  3. Wernicke’s area = Lies in dominant posterior part of temporal lobe Q. (superior temporal gyrus –LQ 2012)
  4. It is sensory speech area.
  5. Arcuate fibers = They connect the two speech areas.

Physiology of speech:


Spoken words  ears auditory area in temporal lobe via 8th nerve Wernicke’s area where speech is understood Message go to Broca’s area via Arcuate fiber Broca’s area is a motor speech area which gives command to vocal cord and lip area in the motor cortex speech is spoken.


  1. Damage to the Primary Auditory Cortex in humans leads to a loss of any awareness of sound in the ipsilateral side (LQ 2012), but an ability to react reflexively to sounds remains as there is a great deal of subcortical processing in the auditory brainstem and midbrain even in those cases having bilateral primary auditory cortex.
  2. Broca’s area involvement = motor aphasia (Verbal comprehension impaired) – Speech out flow and fluency is lost. There is no neologism but repetition may be lost.
  3. Wernicke’s area involvement – Speech understanding is lost. There by patient speaks senselessly but repetition may be lost.

Table: Characteristics of dysphasia (Ref. Hari. 18th ed., Table 26.1 Pg- 203)







Anterior (Broca)





Posterior (Wernicke)

Normal / Increased




Arcuate fasciculus conduction)





Fronto – parietal (global)

Very reduced





Extra Edge: Nominal aphasia is seen in metabolic encephalopathy. It is also an early feature of Alzheimer disease.Q


Broca’s aphasia

Wernicke’s aphasia

Lesion site

• Lesion in Broca's area (inferior frontal gyrus)

· Lesion lies in Wernicke's area (supramarginal gyrus) of the parietal lobe and upper part of temporal lobe


• Lesion is due to occlusion of superior br. of middle cerebral art.

· Lesion is due to occlusion of inferior division of middle cerebral artery.


• Comprehension is preserved (except grammar)

· Comprehension is impaired


• Decreased: speech is not fluent, laboured, dysarthric, and interrupted with many word finding pauses. It is telegraphic but informative.

· Preserved or increased: Speech fluent but is highly paraphasic and associated with neologisms (Jagron Aphasia)


• Impaired

· Impaired


• Impaired

· Impaired


• Absent

· Present


• Insight into condition is preserved

· Not preserved


Extra Edge:

  1. Pure alexia = Comprehension impaired only for reading
  2. Pure words deafness = Comprehension impaired only for spoken words (Ref. Hari. 18th ed., Pg- 205)

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