Learning Objectives.

Transcription

1 Emilie O Neill, class of 2016

2 Learning Objectives 1. Describe the types of deficits that occur with lesions in association areas including: prosopagnosia, neglect, aphasias, agnosia, apraxia 2. Discuss the concept of brain asymmetry as it relates to language. 3. Describe the functions of the prefrontal cortex and the effects of lesions. 4. Describe the location and functions of the limbic system. Chris Cohan, Ph.D. Dept. of Pathology/Anat Sci Jacobs School of Medicine

3 Topics To Discuss Consider complex cortical functions and their deficits Tactile association area and neglect syndrome Language areas and disorders Prefrontal area and executive function Awareness lesions in some cortical areas are not accompanied by awareness of the deficits Asymmetry some functions reside in only 1 hemisphere

4 Cortical Areas and Deficits AREAS DEFICITS Primary Sensory/Motor Areas loss of perception touch, pain, vision, hearing, move or movement Sensory/Motor Association Areas agnosia, apraxia Integrative Areas cognitive loss language, reasoning, problem solving, emotional control Agnosia inability to use sensory information in complex ways although perception is preserved. Apraxia inability to perform complex movements without weakness or paralysis.

5 Cortical Areas and Deficits Agnosia With damage to sensory association areas while the primary sensory area is intact, patients can perceive simple aspects of a sensory stimulus, but complex aspects are impaired. A patient who can feel when they are touched, but CANNOT: identify an object placed in their hand identify a number drawn on their palm

6 Cortical Areas and Deficits Apraxia Damage to sensory or motor association areas produces an inability to perform familiar movements on demand in the absence of sensory or motor impairment. A patient who is not paralyzed, but CANNOT: walk with the normal stepping pattern show you the motion to brush their teeth demonstrate how to write their name

7 Cortical Areas and Deficits In lesions that cause anosognosia, patients are typically unaware of their deficit. These lesions cause selective and restricted loss of self awareness for a specific modality, but maintain awareness for other modalities. In some cases this requires bilateral damage to same area in each hemisphere.

8 Visual System Occipital/Temporal Lobes the where and what of objects Parietal Dorsal Path - where: analysis of object position and motion. Bilateral lesions: motion agnosia what where Temporal Ventral Path - what: analysis of form, color, faces, written words. Lesions: color/form agnosia, prosopagnosia, reading agnosia Large Occipital Lobe lesions: cortical blindness, Anton s syndrome. loss of awareness

9 Tactile System Parietal Lobe tactile recognition of objects attention to personal space integration of tactile/visual/language information; eye-hand coordination tactile language visual Lesions: astereognosis, agraphesthesia, EDSS, apraxia, neglect

10 Neglect Syndrome Model Patient Inattention to contralateral side of the external world and body. Patient disregards visual, tactile, auditory stimuli from one side. Patient is unaware of deficit. Lesion usually on right, but can also occur on left. May involve a visual deficit (left homonymous hemianopia).

11 Language Temporal/Frontal Lobes Language Comprehension (sensory): Temporal Lobe - Wernicke s area meaning of sound and understanding language Wernicke s Area word comprehension Speech (motor): Frontal Lobe - Broca s area Word Memory: Temporal lobe Integrative areas: reading - visual/language braille - tactile/language Broca s Area speech

12 Lesions Affecting Language Aphasia is a disruption of language capability separate locations = differential effects Wernicke s Aphasia inability to understand meaning of words Fluent speech but nonsense meaning Unaware of deficit Broca s Aphasia understands words Nonfluent can t vocalize; word use affected Aware of deficit Superior longitudinal fasciculus connects Wernicke s and Broca s areas lesions conductive aphasia (inability to repeat words spoken to patient)

13 Language Shows Brain Asymmetry Surgery was performed on a group of patients with severe epilepsy in the 1960s. The cerebral hemispheres were disconnected by cutting the corpus callosum to prevent the spread of abnormal electrical activity from one hemisphere to the other. Studies (split brain experiments by R. Sperry/nobel prize and M. Gazzaniga) performed on these patients made the startling discovery that language was localized to the LEFT hemisphere in most of the patients.

14 Hemispheric Asymmetry Split brain experiments: hemispheres surgically isolated in patients with severe epilepsy stimuli (tactile, visual) presented to only one hemisphere without communication to other hemisphere what do patients report? what are innate capabilities of each hemisphere?

15 Split Brain Experiments Visual stimuli presented to: RT visual field - patient names object LT visual field - patient says nothing Patient draws object when pencil is placed in LT hand, but does not know why. Patient makes up an explanation for the drawing (confabulation). When the brain is challenged with a situation it cannot explain, it makes up an explanation. Confabulation also occurs in patients with memory disorders.

16 Language Shows Brain Asymmetry Language localized in Left hemisphere in most adults Related to handedness: RT handed - 96% have language in LT brain LT handed - 70%LT, 15%RT, 15%bilateral people - both languages in same hemisphere. Lesions may preserve one language but impair the other.

17 Language Asymmetry What about the RIGHT hemisphere Controls the emotional content of language intonation, singing Because these features of spoken language are separated to the 2 hemispheres, speech can be affected separately from song, eg people who stutter can sing normally. This property is used therapeutically to retrain Broca aphasics.

18 Unilateral brain lesions - tendency for clinical asymmetry: LT lesion RT lesion Space awareness neglect (parietal) Language speech aphasia (Broca) comprehension aphasia (Wernicke) Mood depressed (frontal lobe) cheerful (frontal lobe)

19 Frontal Lobe Motor Association Areas Planning and integration of movement Supplementary Motor Area Premotor Cortex Lesions cause apraxia.

20 PreFrontal Cortex Executive Functions Planning Reasoning Problem Solving Judgment Decision making Story of Phineas Gage 1850 s railroad worker who injured frontal lobe and survived. Provided first information about functions of frontal lobe.

21 PreFrontal Cortex Dorsolateral area long-term planning, problem solving, reasoning.. Ventromedial/Orbitofrontal area awareness of social context of behavior emotional control Lesions: cognitive deficits in reasoning, judgment, problem solving, control of emotions, disinhibition.

22 Limbic System Medial portion of frontal, parietal, temporal lobes Emotion and memory processing subcallosal, cingulate, parahippocampal gyri, amygdala, hippocampus A transitional area between cortex and structures that control visceral function.