1. Venous system

2. Cerebral venous system
Superficial system:
Drains into the venous synuses
Central system
Drain in a large, short venous trunk – the great vein of Galien
Basal system
Drains the blood into the basilar vein and then to the great vein of Galien
Jugular veins

3. Cerebral venous trombosys
Causes:
Infectious – significantly decreased since antibiotics
Local
General
Non infectious
Local: trauma, surgical interventions, tumors, arterialtrombosys, malformations
General: surgicale, pregnancy, post partum/post abortum, drugs, dehydration, advanced liver or kidney disease
Idiopatic

4. Cerebral venous trombosys
Venous synus thrombosis:
Increased pressure in the preceding veins (depending on the anastomosys system)
increased intracranial pressre
Superior longitudinal synus: role in resorbtion of the CSF
Cerebral veins thrombosys
Secondary hemorrhage is more frequent
Cerebral edema, venous infarcts
Seizures

5. Cerebral venous trombosys
Clinical picture:
Increased intracranian pressure (headache, nausea, papillary edema, consciousness abnormalities)
Focal or generalized seizures
Meningean syndrome
Focal signs
Septic CVT: fever, other signs of severe infection

6. Cerebral venous trombosys
Cavernous synus thrombosys
Staphilococcus infections of the face, orbitary, synuses, teeth other ENT infections
Trauma
Usually the clinical picture is marked by the septic syndrome
Venous stasis:
Palpebral edema, chemosis, exoftalmia
VI-th and then IIIrd, IV-th, and ophtalmic ramus of the Vth nerves palsies
Often clinical signs are bilateral – the 2 synuses are conected

8. Cerebral venous trombosys
Investigations
CT, MRI
Thrombus image
Empty vessel (CT with contrast substance)
Infarctus or hemorrhages images
Arteriography
CSF analysis – differential diagnosys of an infection
EEG, funduscopy
Treatment:
Etyologic treatment
Antithrombotic treatment (anticoagulants)
Treatment of cerebral edema, raised intracranian pressure, seizures

9. Brainstem alternate syndroms

10. Medullary alternate syndromes
A combination of the following, in various degrees, depending on the exact position and size of the lesion:
On the same side with the lesion
Nucleus ambigus, vagus nerve nucleus, hipoglossal nerve nucleus, accesory nerve nucleus
Palatal weakness, bitonal voice,
Tongue atrophies
sternocleidomastoidian and trapesus muscle palsy,
On the opposide side
Loss of temperature and pain sensation
Hemiparesis

11. Lateral medullary syndrome (Wallenberg syndrome)
This is the commonest of the brain stem strokes
Vertebral artery or postero-inferior cerebellar artery
Sudden onset
Intense vertigo, vomit, balance problems, hiccup
Most of the times: favourable evolution

12. Lateral medullary syndrome (Wallenberg syndrome)
On the same side with the lesion:
Involvement of the descending nucleus and tract of Vth nerve results in loss of pain and temperature sensation on the face
Vestibular syndrome
Swallowing problems, palatal weakness and dysphagia - bitonal voice (involvement of the nucleus ambiguus, IXth, Xth, XIth nerver palsy)
Horner’ syndrome (involvement of descending autonomic fibers )
Involvement of the inferior cerebellar peduncle (restiform body) causes ipsilateral ataxia
On the opposite side:
Loss of pain and temperature sensation
Sometimes discrete hemiparesis

13. Infarction of the base of the pons
In bylateral lesions: corticospinal and corticobulbar tracts in the basis pontis are interrupted
Locked in syndrome
Tetraplegia, billateral facial palsy, billateral palsy of the abducens nerve
Vertical gaze is maintained
Consciousness/higher functions are maintained, but the patient is unable to speak or move
Lesion spares the reticular formation above the caudal pons, and therefore the patients remain awake
The only way to communicate with these unfortunate patients is to ask them to move their eyes in response to questions.

14. Millard-Gubler syndrome (pontine inferior)
On the same side with the lesion
Peripheral facial palsy
External oculomotor (VIth nerve) palsy
On the opposite side
hemiplegia

15. Pontine lesions Lesions of the sixth nerve nucleus
paralysis of gaze to the side of the lesion.
Internuclear palsy (fibers from the opposite 6th nerve nucleus are involved as they cross to the MLF, there is also weakness of the ipsilateral medial rectus muscle).
The ipsilateral seventh nerve can be involved since its fibers course around the sixth nerve nucleus.
Involvement of the medial lemniscus
contralateral loss of position and vibration sense
descending corticospinal fibers in the base of the pons
contralateral hemiparesis

16. Midbrain syndromes: Weber syndrome
Are involved
the descending corticospinal and corticobulbar fibers in the cerebral peduncle, and
the fibers of the third nerve that traverse the peduncle on exiting the midbrain.
On the opposite side: hemiparesis
On the lesion’s side: third nerve palsy (ptosis, inability to move the eye up, down or medially, and [if fibers from the Edinger-Westphal nucleus are involved] pupillary dilitation).

17. Red nucleus syndromes
Third nerve palsy on the same side, cerebellar syndrome on the opposite side, chorea, thalamic sensory syndromes
Chorea
Benedikt's syndrome
homolateral third nerve palsy
contralateral ataxia,
midbrain stroke involving the third nerve as it travels near the red nucleus. A lesion of the red nucleus interrupts fibers from the opposite cerebellar hemisphere (dentate nucleus of the cerebellum superior cerebellar peduncle crossing in midbrain red nucleus VA/VL thalamus).

18. Cerebral lobe syndromes

21. Frontal lobe

22. Frontal lobe Highest level of brain evolution
Involved in many functions
Lesions in different parts lead to different syndromes

23. Frontal lobe

24. Frontal lobe syndrome
Lesions of the motor area lead to motor deficits of the opposite half of the body
Irritative lesions – jacksonian motor seizures
Lesions of premotor areas – less important motor deficit
Irritative lesions in premotor areas – “adversive” seizures, or supplementary motor area seizures
Supplementary motor area seizures: cessation of all activity, tonical contractions of proximal muscles, repetitions, pallilalia
Premotory areas lesions: diminishment of spontaneous movements, delay of voluntary actions (movements), eventually hyopkinesia, akinesia, tremor
Forced prehension
Gait and posture abnormalities; frontal ataxia

25. Frontal lobe syndrome Prefrontal areas lesions
Alteration of personality
Diminishment of spontaneous activity - the patient does not feel the need to do anything, is not able to plan the future events, may be agitated
Attention deficits – memory is normal, but the patient doesn’t bother to use it
Loss of abstract thinking
Perseveration
Afffective changes – either apathic, “flat”, either excessively exuberant and childish; may show lack of inhibition, eventually sexually improper actions
Gislason TB, Sjogren M, Larsson L, et al; The prevalence of frontal variant frontotemporal dementia and the frontal lobe syndrome in a population based sample of 85 year olds.;J Neurol Neurosurg Psychiatry 2003 Jul;74(7): [abstract]

26. Frontal lobe syndrome Prefrontal dorsolateral cortex lesions
Diminished fluency (verbal & nonverbal), reasoning problems, reduction of spontaneous responses inhibition, perseveration, attention deficits
Orbitofrontal cortex lesions – desinhibition, anosmia
Mezial frontal cortex, anterior cingullary cortex lesions – apathy, abulia, memory impairments

27. Cognitive function testing in frontal lobe lesions
MMS does not approach these problems
Frontal lobe tests:
“go-no go” tests – patient is told to lift 2 fingers, but the evaluator lifts only 1
Speech fluency – patient is asked to produce as many words he can starting with letter “Z” – normally more than 8 words/ 1 min
Motor tests for perseveration – patient is asked to execute series of 3 movements (fist, edge-palm tests – Luria)

28. Parietal lobe

29. Parietal lobe Anterior somatosensory area, posterior association area
4th neuron of sensory tracts (3, 1, 2 areas – primary somatosensory cortex
5, 7, 39, 40 areas – somatosensory association areas; areas 5 and 7 are important for stereognosis
Parietal regions appear when the singers are used for more than just mobility (catching, throwing)

30. Parietal lobe syndromes
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

31. 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

32. 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

33. Parietal lobe syndromes
Gerstmann syndrome (left angulary girus)
Digital agnosia
Left-right confusion
Agraphia
Acalculia

34. Parietal lobe syndromes
Balint syndrome (bilateral posterior parietal lesions)
Patient looks only at 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

35. Parietal lobe

36. Constructive apraxia

37. Adaptative possibilities of parietal lobes – blind boy “reads” with the tip of his nose

38. Temporal lobe

39. 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

40. Sindroame de lob temporal
Lezarea lobului temporal
tulburari de auz, echilibru, gust, miros, limbaj, vedere, memorie, comportament alimentar, comportament sexual.
Convulsiile cu originea in aceste arii se manifesta ca si asocieri de tulburari ale ratiunii, halucinatii, comportament anormal, detasat sau violent, necontrolabil
Afectarea auzului – lezarea ariei 41; leziune unilaterala – hipoacuzie; leziuni bilaterale – surditate corticala. Leziunile iritative (epilepsie temporala) apar iluzii auditive, halucinatii auditive
Tulburarile de echilibru – atacuri de vertij, uneori cu ataxie
Tulburarile de gust si miros – halucinatii olfactive pot apare ca parte a crizelor epileptice. Distrugerea ariei olfactive din uncusul hipocampic si extinderea leziunilor spre girusul hipocampic duc la anosmie. Halucinatiile olfactive pot uneori precede convulsiile (aura)
Afectarea vizuala – hemianopsie, afectarea memoriei vizuale
Tulburari de vorbire de tip afazic receptiv (afazie Wernicke) – leziuni ale ariei posteroinferioare a girusului temporal superior stang

41. Sindroame de lob temporal
Tulburari de memorie
Tulburarile memoriei recente – leziuni hipocampice inferioare bilaterale.
Lezarea bilaterala a corpilor mamilari duce la afectarea memoriei pe termen scurt
Afectarea memoriei pentru cuvinte
Afectarea memoriei pentru cuvinte in leziunile hipocampice inferioare bilaterale
Afectarea memoriei de lunga durata – leziuni mamilotalamice sau leziuni corticale bilaterale
Inmagazinarea de elemente noi si intelegerea acestora se realizeaza prin intermediul circuitului lui Papez (hipocamp, corpi mamilari, talamus, girus cinguli)
Tulburari ale comportamentului alimentar si sexual – nu numai in leziuni ale lobului temporal, ci si in leziuni hipotalamice
Epilepsia de lob temporal
Diagnostic electroencefalografic
Halucinatii psihosenzoriale simple sau complexe, episoade de afazie, halucinatii olfactive sau auditive
Tulburarile de recunoastere si amintire – déjà vu, deja pense, jamais vu

42. 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 memory.

43. Sindromul Kluver Bucy Heinrich Kluver si Paul Bucy, 1939
Lobectomie temporala bilaterala – prima dovada experimentala a implicarii circuitului luii Papez in expresia emotionala
Lipsa de afect, agnozie vizuala, expresie sexuala nediscriminata, pierdere severa a memoriei

44. Occipital lobe

45. Lobul occipital O mica parte a portiunii dorsolaterale a emisferelor
Functiile sunt legate de vedere
Perceptie vizuala
Recunoastere in relatie cu spatiul si timpul
Ariile 17, 18 si 19 Brodmann
Aria 17 (striata) este localizata la nivelul scizurii calcarine si in vecinatatea acesteia; este centrul de receptie al informatiei vizuale (culoare, dimensiuni, forma, miscare, iluminare, transparenta)
Aria 18 (parastriat) si aria 19 (peristriat) ocupa restul suprafetei interemisferice la nivel occipital, avand rol de cortex de asociatie
Tulburarile care rezulta din lezarea lobului occipital pot fi de natura iritativa sau datorate unui deficit, cu simptomatologie uni sau bilaterala

46. Sindroame de lob occipital
Leziuni iritative:
Halucinatii vizuale – simple (elementare) sau complexe, avand aspecte senzitive si cognitive
Halucinatiile elementare includ stele, flashuri luminoase, culori, lumini forme geometrice (cercuri, patrate, hexagoane), care pot fi mobile sau stationare (zigzag, oscilatii, vibratii, pulsatii)
Halucinatiile complexe include obiecte, persoane, animale de dimensiuni normale, foarte mici sau foarte mari. Pacientul poate constientiza natura ireala a acestora sau poate fi convins ca sunt reale.
Iluzii vizuale (metamorfopsia) – distorsionarea obiectelor (forma, dimensiuni, culoare, miscare)
Imaginile pot sau nu sa evoce amintiri vizuale. Efectul cumulat este asemanator cu starea de vis care apare in epilepsia temporala.
Micropsie, macropsie sau megalopsie, obiecte in miscare spre subiect, alungite, umflate, modificari ale dimensiunilor orizontale sau verticale
Coloratii iluzorii (erithropsia), lipsa culorilor (acromatopsia), vedere inversa, iradierea contururilor, poliopie (un obiect apare multiplicat), diplopie monoculara, iluzii de miscare a obiectelor stationare
Pierderea vederii spatiale, reaparitia periodica a unor imagini dupa ce ele au incetat sa se mai afle in campul vizual (palinopie sau palinopsie), o falsa orientare a obiectelor in spatiu (allestezie optica)
Epilepsia de lob occipital – halucinatii vizuale elementare, care se misca sau nu in campul vizual

47. Sindroame de lob occipital
Sindroame de deficit
Agnozia pentru culori – pierderea perceptiei corecte pentru o culoare, imposibilitatea denumirii culorilor, a identificarii lor
Leziunile distructive unilaterale duc la hemianopsie controlaterala omonima (pierderea partiala sau completa a vederii care se proiecteaza in aria corticala occipitala primara
Cecitatea corticala apare atunci cand ambele arii vizuale primare din lobul occipital sunt lezate.
Pacientul nu este capabil sa proceseze informatia vizuala si se comporta ca si in cazul unei cecitati periferice.
Unii pacienti incearca totusi sa se comporte ca si cum ar vedea (nu isi recunosc cecitatea). Acest tip de cecitate corticala se numeste sindromul Anton, si are asociate leziuni parietale si neglijare senzitiva, in unele cazuri si pentru alte modalitati ale sensibilitatii.

48. Sindroame de lob occipital
Leziunile ariilor 18 si 19 din emisferul dominant duc la agnozie vizuala pentru obiecte (acestea pot fi recunoscute prin intermediul altor simturi); de obicei este insotita de agnozie verbala si hemianopie omonima.
Dislexia – tulburari de recunoastere a cuvantului scris. Cecitatea pentru cuvinte este o tulburare rara (cortexul vizual primar este intact, leziunea se afla in cortexul occipital de asociere pe partea stanga)
Prosopagnozia – leziunile sunt localizate in regiunile de asociere ventromediala si occipitotemporala; frecvent insotita de agnozie pentru culori
Sindromul Balint
Lezarea bilaterala a lobilor occipitali, cel mai frecvent in ariile de granita (19 si 17) ale regiunii parieto occipitale
Imposibilitatea dirijarii corecte a oculomotricitatii in timpul explorarii spatiului; imposibilitatea privirii voluntare si a scanarii spatiului periferic, imposibilitatea de a apuca si de a atinge un obiect cu ghidare vizuala.
Inatentia vizuala care afecteaza in primul rand periferia campului vizual