Parietal lobe
Parietal lobe
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Anterior somatosensory area,
posterior association area
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4th neuron of sensory tracts (3, 1,
2 areas – primary somatosensory
cortex
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5, 7, 39, 40 areas – somatosensory
association areas; areas 5 and 7
are important for stereognosis
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Parietal regions appear when the
fingers were used for more than
just mobility (catching, throwing)
Parietal lobe syndromes
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Controlateral hemihypestesia (diminished sensation)
Astereognosis (5 & 7 areas lesions)
Sensory epilepsy (paresiae and sometimes paroxistical pain)
Asomatognosia (left hemisphere lesions lead to one side
asomatognosia, anosognosia, anosodiaforia, neglect of left body
half)
• Right parietal lobe – spatial component of activities
– Apraxia – loss of the ability to execute or carry out learned purposeful
movements, despite having the desire and the physical ability to perform
the movements
– Finger agnosia
– Left-right agnosia
Parietal lobe syndromes
• Left parietal lobe – symbol and experiences comprehension
– ideomotor (inability to carry out a motor command or a learned gesture, for
example, "act as if you are brushing your teeth" or "salute")
• limb apraxia when movements of the arms and legs are involved,
• nonverbal-oral or buccofacial (inability to carry out facial movements on command,
e.g., lick lips, whistle, cough, or wink),
– ideational (inability to create a plan for or idea of a specific movement, for
example, "pick up this pen and write down your name")
– Inability to use the informations on spatial relations
• Constructive apraxia
• Topographic agnosia
• Prosopagnosia
Parietal lobe syndromes
• Speech problems – frequently
associated with writing problems
• Motor abnormalities (diminishment
of spontaneous movements, unstable
hand, syncynesia)
• Balance problems
• Taste problems (area 43)
• hemianopia
Parietal lobe syndromes
• Gerstmann syndrome
(left angulary girus)
• Digital agnosia
• Left-right confusion
• Agraphia
• Acalculia
Parietal lobe syndromes
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Balint syndrome (bilateral posterior parietal lesions)
– Patient looks only at 35-40 degrees to the right, and
describes only the objects in that area
– Can look at only one object a time
– Neglect of left hemispace
– Tactile functions impairment
– Visual or tactile agnosia
– Apraxia
– Speech problems (alexia, aphasia)
– Dyscalculia
– Immediate memory impairment
– Body scheme abnormalities
– Left-right confusion
– Problems with space orientation
– Eye movements problems
Parietal lobe
Constructive apraxia
• Adaptative
possibilities of
parietal lobes – blind
boy “reads” with the
tip of his nose
Temporal lobe
Temporal lobe
• Below the sylvian sulcus, extends up to the limits of the parietal and
occipital lobes
• Primary and secondary auditory areas (41, 42), association areas (38, 20,
21, 22);
– Taste (area 38)
– Areas 41 and 42: perception and comprehension of sounds, comprehension of words
• Lymbic system (hyppocampic uncus, hypocampus, girus cinguli, subcallosal
areas, olfactory areas)- emotions and affect
• Optic radiations
• Left temporal lobe – comprehension and recognition of words, language
• Right temporal lobe – intonation, music
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Temporal lobe disfunction
Lezarea lobului temporal
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Functions in hearing, balance, taste, smell, spoken language, sight, food intake, sexual behaviour
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Temporal seizures appear as asoociations of halucinations, consciousness/reason, abnormal
behaviours (violent or detached, uncontrollable)
Hearing disfunction – area 41 lesions; unilateral lesions – hipoacusia; bilateral lesions –
cortical deafness
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Iritative lesions – auditory ilusions/halucinations
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Balance disfunctions – paroxistical vertigo, sometimes ataxia
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Taste and smell disturbances – olfactory hallucinations (sometimes as an aura); anosmia
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Visual disturbances – hemianopia, visual memory impairment
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Speech disturbance – sensory aphasia (Wernicke) – lesions of the posteroinferior
parts of the left superior temporal gyrus
Temporal lobe syndrome
• Memory impairment
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Impairment of recent memory – bilateral inferior
hippocampic lesions
Long time memory impairment – mammilothalamic
lesions, bylateral cortical lesions
Storing of new memories and their comprehension
depends on the Papez circuit (hippocampus, mammilary
bodies, thalamus, gyrus cinguli)
• Abnormal eating and sexual behaviours –
both in temporal lobe lesions and hypothalamic
lesions
• Temporal lobe epilepsy
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Simple or complex psycho-sensorial hallucinations
Episodic aphasia
Olfactory or auditory hallucinations
Mnestic (recognition and recall) disorders– déjà vu, deja
pense, jamais vu
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Papez circuit
James Papez in 1937
One of the major pathways of the limbic system
Chiefly involved in the cortical control of emotion.
Role in storing memories
Kluver-Bucy syndrome
• Heinrich Kluver si Paul
Bucy, 1939
• Bilateral temporal
lobectomy – proof of the
role of the Papez circuit in
emotional expression
• Lack of affect, visual
agnosia, indiscriminate
sexual expression, severe
memory loss
Occipital lobe
Occipital lobe
• Part of the dorsolateral face of the hemispheres
• Brodmann areas 17, 18, 19
• Sight
– Visual perception
– Recognition in relation to space and time
– Area 17 (striate) – center of visual information perception - color, shape, dimansion,
light, transparency, movement
– Area 18 (parastriate) and area 19 (peristriate) – the rest of interhemispheric surface
in the occipital lobe
• Association cortex
• Disfunctions of the occipital lobe can be irritative/destructive, uni- or billateral
Occipital lobe syndromes
• Irritative lesions:
– Simple or complex visual halucinations
• Elementary hallucinations: light flashes, colours, gemoetrical shapes, mobile or
stationary
• Complex hallucinations – objects, persons, animals of normal or abnormal
(smaller or larger) dimensions
• The patient is either aware of the false nature of these experiences, but he
might also be convinced that they are real
– Visual illusions (metamorphopsia) – distortions of objects (shape, size,
colour, movement)
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Images may arouse visual memories
The effect can be similar to "dream state" seen in temporal epilepsies
Mycropsia, macropsia, moving objects, difformed objects
Erithropsia (abnormal colours), lack of colour (acromatopsia), inverted vision,
polyopia, irradiation of contours, illusions of movement of stationary objects
• Loss of stereoscopic sight, periodic reapparence of visual images after they are
no longer in sight (palinopia)
• Occipital lobe epilepsy – elementary visual hallucinations,
fixed or mobile in the visual field
Occipital lobe syndromes
• Destructive lesions/visual deficits
• Colour agnosia – loss of correct colour perception, inability to
name/recognize colours
• Unilateral lesions - controlateral homonimous hemianopia (partial or
complete loss of sight in the visual field projecting in the primary occipital
visual area)
• Cortical blindness – both primary visual areas are lesioned
– Patients cannot process visual information and behave as in a peripheral
blindness
– Some patients try to behave as if they were able to see (do not aknowledge the
blindness)
– Anton syndrome – associates parietal lesions and sensory neglect, sometimes for
other types of sensory information
Occipital lobe syndromes
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Lesions in the areas 18, 19 of the dominant hemisphere : visual agnosia
(objects can be recognized through other senses, but not sight); ussualy
associated with verbal agnosia ant homonimous hemianopia
Dislexia – impairde written words recognition
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Word blindness is rare (intact primary visual cortex, but lesions in the association visual cortex
in the dominant hemisphere)
Prosopagnozia – lesions of the associations areas (ventromedial and
occipitotemporal); frequently associated with colour agnosia
Balint syndrome
– Bilateral occipital lobe lesions, most often in the border areas (19 and 17) of the
parieto-occipital region
– Failure too properly direct the oculomotor function in exploration of space
– Inability to look voluntarily into and scan the peripheral field, failure to grasp or
touch an object under visual guidance
– Visual innatention that mainly affects the periphery of the visual field
Migraine
Migraine
• Periodic paroxysmal attack of
headache
• Familial / hereditary;
• Females
• Usually starts during
adolescence
• Usually normal imagistic
aspects
Clinical features of headache
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Hemicrania
Duration (untreated) - 4 – 72 h
Pulsatile
Medium / severe intensity
fono- / foto- / osmofobia
Frequently nausea and/or
vomiting
• Autonomic phenomena (pallor,
mydriasis, elevated blood
pressure, conjunctival
hyperemia, pappiloedema)
• Accentuated by physical activity
• 3-5 such episodes in history
Classification
1.1 Migraine without aura
1.2 Migraine with aura
1.2.1 Typical migraine with aura
1.2.2 Typical aura but no headache
1.2.4 familial hemiplegic migraine
1.2.5 sporadic hemiplegic migraine
1.2.6 basilar migraine
1.3. paroxistical childhood syndromes – migraine precursors
1.3.1 repeated vomiting
1.3.2 abdominal migraine
1.3.3 paroxistical benign vertigo of chilhood
1.4 ophtalmoplegic migraine
1.5. migraine complications
1.5.1 chronic migraine
1.5.2 status migrainosus
1.5.3 prolonged aura but no infarct
1.5.4 migraine associated infarctus
1.5.5 migraine triggered seizures
Physiopathological mechanisms
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Vasomotor theory
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Theory of vascular neuroactive substances
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During the acute phase of migraine kinines,
acethylcholine, substance P induce a
vasodilatator effect an hyperalgia
Diencephalic theory
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Central blood flow is reduced in some
territories during the prodromal phase
In the acute phase there is vasodilation and
arterial distension
Adventitial edema
Initial disturbance in the hypothalamic
structures and limbic cortex that activate
noradrenergic mechanisms
Reduction of serotonin activity
Allergic theory
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Association with coryza, frequent urticaria,
Quincke oedema, bronchial asthma attacks
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Cortical depression theory
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Depolarization wave that spreads on the
cortex from the occipital areas at a speed
of 3-5 mm/min.
Starts with an excitation wave followed by
a long period of neuronal depression that
associates metabolic disfunctions and
diminished local blood perfusion
• Integrative theory
– Unitary mechanism that
explains the apparition of
migraine attacks
– Unifies all the othe theories
– Stress, strong light, carotid
artery dilation maight
activate specific structures in
the midbrain
Treatment – acute phase
• Triptanes: s.c., oral, nasal
spray
– Sumatriptan, naratriptan,
rizatriptan
• Aspirin, paracetamol in
high doses
• Nonsteroidal
antiinflamatory drugs
(Ibuprofen, Naproxen,
Diclofenac, Tolfenamic
acid, Indomethacin
suppository
• When to treat?
– EARLY
– Within 2 hours
– Treatment during
prodrome or aura is even
more effective
Treatment: Triptans
• First line
– More effective
– Less nausea
• Contraindications
– CAD
– Cost
• Routes
– Oral
– Intranasal
– Subcutaneous
Treatment: Triptans
• Mechanism of Action
– Selective serotonin agonist
– 5HT1B/1D
• Pharmacokinetics/dynamics
– Both long and short acting available
– Long acting more effective during aura but take
longer to act
– Short acting have more side effects
Treatment: Adjuncts
• Anti-emetics
– Metoclopromide both as adjunct and monotherapy
– Ondansetron IV/oral/ODT
• Caffeine
– Rebound
• Steroids
– Dexamethasone
– Prednisone
Treatment: Non-Pharmacologic
• Behavioral
– Shown to be effective
• 30-50% reduction of migraine frequency
• Modalities
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Relaxation training
Thermal biofeedback with relaxation training
Electromyogram biofeedback
Cognitive behavioral therapy
– No data to guide selection of modality…
Treatment: Non-Pharmacologic
• Diet
– Some benefit to elimination diets
– 20% of patients report dietary triggers
– Common triggers:
Caffeine withdrawal
Packaged meats
MSG
Dairy
Fatty foods
Aged cheese
Red wine
Beer
Champagne
Chocolate
Background therapy
• If there are more than 2 attaccks/month
• Beta-blockers
• Antiepileptics: valproic acid, topiramate
• Antiserotoninergic drugs
• Tricyclic antidepressants