Case Studies PDF

NEUROPSYCHOLOGY - CASE STUDIES Case 1: WILL BE COMING FOR EXAM A patient has been referred to you, with symptoms of memory and attention impairment, loss of emotional control and repetition of already completed actions. In addition, MRI shows frontal lobe lesions. A) Disc...

NEUROPSYCHOLOGY - CASE STUDIES Case 1: WILL BE COMING FOR EXAM A patient has been referred to you, with symptoms of memory and attention impairment, loss of emotional control and repetition of already completed actions. In addition, MRI shows frontal lobe lesions. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. Diagnosis and Neuroimaging Techniques Possible Diagnosis: ​ Dysexecutive Syndrome or Frontal Lobe Syndrome. The symptoms and lesion location suggest it. These conditions involve disruptions to the brain’s executive functions due to frontal lobe damage. ​ Frontal lobe functions include planning, decision-making, emotional regulation, working memory, and inhibitory control. Damage here leads to behavioral disinhibition, reduced problem-solving, and emotional instability. The frontal lobe is crucial for executive functions such as decision-making, planning, reasoning, problem-solving, and emotional regulation. It also governs voluntary motor activity, language production (via Broca's area), and social behaviors. Frontal lobe syndrome arises from injury or dysfunction in this region, leading to diverse effects like impaired judgment, apathy, difficulty concentrating, impulsivity, and personality changes. Patients may struggle with goal-directed actions, exhibit inappropriate behaviors, or have poor emotional control. Depending on the severity, these deficits can significantly impact daily functioning, relationships, and quality of life, requiring tailored rehabilitation and therapeutic interventions. - Introduced by Alan Baddeley - Previously known as “frontal lobe syndrome” - Deficits are not solely attributed to frontal regions - Cognitive symptoms include: memory, planning & reasoning impairments, attention deficits, difficulty with consequences, confabulation (Confabulation is a type of memory error in which gaps in a person's memory are unconsciously filled with fabricated, misinterpreted, or distorted information) - Emotional symptoms include: loss of inhibition & emotional control - Behavioral symptoms include: poor impulse control, inappropriate use of objects, repetition of already completed actions. Symptoms: Memory and attention impairments Emotional Dysregulation 1 Perseveration (repetition of completed actions) MRI (Magnetic resonance imaging) shows frontal lobe lesions. Other Neuroimaging Techniques: 1.FMRI - Functional magnetic resonance imaging. Helps assess functional disruptions in brain activity, such as connectivity issues in executive networks. It measures the small changes in blood flow that occur with brain activity. It may be used to examine which parts of the brain are handling critical functions, evaluate the effects of stroke or other disease, or to guide brain treatment. 2.Diffusion Tensor Imaging (DTI): Tracks white matter damage, particularly in the prefrontal cortex and its connections to other brain regions. 3.PET Scan: Positron Emission Tomography Evaluates glucose metabolism, which can reveal areas of reduced brain activity not visible on standard MRI. While a CT and MRI scan looks at the “form” of structures inside your body, a PET scan looks at their function and shows unusual cellular activity. B) Neuropsychological Conceptualization Assessment: 1. Executive Functions: Tests: WAIS - Wechsler Adult Intelligence Scale and is a widely used intelligence test for adults. It is designed to measure cognitive ability in several areas, such as vocabulary, comprehension, arithmetic, and reasoning skills. WCST - Wisconsin Card Sorting Test. The task has been hypothesised to measure a number of executive functions including attentional set shifting, task/rule switching or reversal, and working memory.relies upon a number of cognitive functions including attention, working memory, and visual processing. MMSE - The Mini Mental State. It is a tool that can be used to systematically and thoroughly assess mental status. It is an 11-question measure that tests five areas of cognitive function: orientation, registration, attention and calculation, recall, and language. TMT - Trail Making Test. To test working memory, tests of speed for attention, sequencing mental flexibility, visual search, and motor function. Stroop Test - To assess unconscious processing. These assess planning, cognitive flexibility, and problem-solving abilities, which are often impaired in frontal lobe damage. 2. Memory and Attention: Tests: Wechsler Memory Scale (WMS-IV), Digit Span, and Continuous Performance Test (CPT). Focus: Working memory and sustained attention deficits. 3. Behavior and Emotional Regulation: Tools: Frontal Systems Behavior Scale (FrSBe), to identify behavioral symptoms like apathy or disinhibition. Rehabilitation: 1.Cognitive Rehabilitation: 2 Use of external aids (calendars, alarms) to support working memory. Problem-solving training and decision-making exercises to enhance executive functioning. 2.Behavioral Interventions: Impulse control strategies and cognitive-behavioral therapy (CBT) to improve emotional regulation. 3. Family Training: Educating caregivers to manage emotional outbursts and repetitive behaviors. Case 2: WILL BE COMING FOR EXAM A patient, about 65 years old, has been referred to you, with symptoms of disinhibition, impulsivity and some symptoms of mild speech impairment. In addition, he has started demonstrating some memory problems too. Neuroimaging shows large impairment in frontal areas, as well as some mild (first only) lesions in temporal areas. Genetic testing showed accumulation of Tau protein. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. Frontal and Temporal Atrophy with Tau Accumulation The frontal and temporal lobes are key regions of the brain responsible for cognitive and emotional functions. The frontal lobe governs executive functions like decision-making, planning, problem-solving, emotional regulation, and voluntary motor activity. It also plays a significant role in social behavior and language production through Broca's area. The temporal lobe processes auditory information, language comprehension (via Wernicke's area), memory formation, and emotional responses. Frontotemporal dementia (FTD), a neurodegenerative condition caused by the abnormal accumulation of tau protein, disrupts these critical functions. Tau protein aggregates damage brain cells, leading to progressive atrophy in the frontal and temporal lobes. This results in distinct symptoms, including personality changes, impaired judgment, loss of empathy, and disinhibition. Patients may also experience language difficulties, such as trouble speaking (aphasia), understanding, or naming objects. Unlike Alzheimer’s, memory impairment is less prominent initially. As FTD advances, it profoundly affects relationships, daily functioning, and independence, often requiring comprehensive care and support. Research on therapeutic strategies to target tau protein is ongoing. A) Diagnosis and Neuroimaging Techniques Possible Diagnosis: Frontotemporal Dementia (FTD) 3  FTD affects the frontal and temporal lobes, leading to progressive behavioral, emotional, and cognitive deficits. Tau protein accumulation is common in FTD and disrupts neuronal functioning. Other Neuroimaging Techniques: 1.FDG-PET: Shows hypometabolism in frontal and temporal regions. 2.Amyloid PET: Differentiates FTD from Alzheimer’s by ruling out amyloid plaques. 3.CSF Biomarkers: Elevated tau levels in cerebrospinal fluid confirm neurodegeneration. B) Neuropsychological Conceptualization Assessment: 1.Executive Functions: wisconsin Card Sorting Test and Stroop Test assesses planning, problem-solving, and cognitive flexibility, often impaired due to frontal lobe involvement. focusing on cognitive flexibility and planning. 2.Social Cognition: Tools: Faux Pas Recognition Test, Theory of Mind tasks. Focus: Empathy deficits and poor understanding of social norms. 3.Language: Boston Naming Test or Semantic Fluency Tasks to evaluate mild speech deficits. and verbal fluency tasks to detect aphasia, semantic deficits, or word-finding difficulties common in FTD subtypes. Memory: Unlike Alzheimer’s disease, episodic memory is relatively spared in early FTD. Tests such as the Rey Auditory Verbal Learning Test can confirm this distinction. Rehabilitation: 1.Behavioral Interventions: - Structured routines to manage impulsivity and disinhibition. - Behavioral activation to address apathy. 2. Language Therapy: Exercises to preserve naming and fluency skills. 3.Caregiver Support: Guidance for managing challenging behaviors and emotional instability. Citations: Rascovsky, K., et al. (2011). “Sensitivity of revised diagnostic criteria for the behavioral variant of frontotemporal dementia.” Brain, 134(9), 2456–2477. Case 3: Chronic Alcoholism and Amnesia A patient with a history of chronic alcoholism, about 70 years old, has been referred to you, with symptoms of amnesia (memory disturbances), confabulation, apathy and some evidence of lack of insight. CT scan shows evidence of neuronal loss and some gliosis in periventricular gray matter. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological 4 impairments. Symptoms: Severe memory impairment, confabulation, apathy, lack of insight. CT shows neuronal loss and gliosis in periventricular gray matter. A) Diagnosis and Neuroimaging Techniques Korsakoff Syndrome (KS): A result of Thiamine deficiency from chronic alcoholism, leading to damage in the mammillary bodies and thalamus. Other Neuroimaging Techniques: 1.MRI: Detects atrophy (gradually decline in effectiveness) in mammillary bodies and thalamus. 2.DTI: Assesses damage to white matter tracts connecting the memory circuit. 3.FDG-PET: Identifies hypometabolism in diencephalic regions. B) Neuropsychological Conceptualization Assessment: 1.Memory: WMS-IV and Autobiographical Memory Interview to test episodic and semantic memory. 2.Executive Functions: WCST Wisconsin Card Sorting Test - to assess planning and problem-solving deficits. Frontal lobe functions: strategic planning, organized searching, utilizing environmental feedback to shift cognitive sets, directing behavior toward achieving a goal, and modulating impulsive responding Rehabilitation: 1.Medical Management: Immediate thiamine replacement. 2.Memory Rehabilitation: External memory aids and spaced retrieval techniques. 3.Behavioral Interventions: Structured, predictable environments to minimize confabulation. Citations: Kopelman, M. D. (1995). “The Korsakoff syndrome.” British Journal of Psychiatry, 166(2), 154–173. Case 4: Transient Amnesia with Headache and Nausea A male patient,75 years old, with a sudden and short period of amnesia (4 hours) has been referred to you for neuropsychological testing. The patient's behavior has been characterized by repetitive questioning and some confusion of basic information. In addition, verbal and non verbal memory of the patient appears affected also. Before this event, Jason has experienced extreme headache and nausea. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. 5 Symptoms: Sudden memory loss lasting four hours, repetitive questioning, confusion, verbal/non-verbal memory deficits. Preceded by headache and nausea. A) Diagnosis and Neuroimaging Techniques Possible Diagnosis: Transient Global Amnesia (TGA): A sudden, temporary episode of memory loss that typically resolves within 24 hours. Core Features: ​ Acute onset of anterograde amnesia with intact self-awareness. ​ Repetitive questioning and difficulty forming new memories. ​ Triggering factors often include stress, migraines, or vascular events. Other Neuroimaging Techniques: ​ 1.​ MRI with DWI (Diffusion-Weighted Imaging): ​ ​ Detects punctate hyperintensities in the hippocampus, particularly in the CA1 region, characteristic of TGA. ​ 2.​ EEG: ​ ​ Rules out epileptic amnesia or transient epileptic syndromes. ​ 3.​ CT Scan: ​ ​ To exclude vascular causes, such as a transient ischemic attack (TIA). B) Neuropsychological Conceptualization Assessment: ​ 1.​ Memory Function: ​ ​ Tests: Rivermead Behavioural Memory Test (RBMT), WMS-IV (Logical Memory and Verbal Paired Associates). ​ ​ Focus: Evaluate recovery of episodic memory. ​ 2.​ Cognition: ​ ​ Mini-Mental State Exam (MMSE) to screen for broader cognitive deficits. ​ 3.​ Emotional Impact: ​ ​ Beck Depression and Anxiety Inventories to address anxiety post-event. Rehabilitation: ​ 1.​ Education and Support: ​ ​ Reassurance that TGA is benign and self-limiting. ​ ​ Counseling to manage anxiety about recurrence. ​ 2.​ Lifestyle Adjustments: ​ ​ Reducing stress and managing migraine triggers. Wechsler Memory Scale Revised (explicit memory test) WAIS - IV (digit symbol test) Wechsler Adult Intelligence Scale Citations: Bartsch, T., & Butler, C. (2013). “Transient global amnesia: Functional anatomy and clinical implications.” The Lancet Neurology, 12(10), 935–944. Case 5: Memory Loss, Anomia, and Hippocampal Atrophy A patient, about 72 years old,has been referred to you, with symptoms of memory loss and signs of agitation. The patient also demonstrates some symptoms of anomia (difficulty in spontaneously finding words during conversation or in naming tasks, and is considered a 6 manifestation of impaired word access or representation), while the MRI shows areas of the hippocampus mostly affected. Labs results show acetylcholine deficiency with serotonergic systems involved too. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. Symptoms: Memory deficits, anomia (word-finding difficulty), agitation. MRI reveals hippocampal atrophy, and lab results show acetylcholine deficiency. A) Diagnosis and Neuroimaging Techniques Possible Diagnosis: ​ ​ Alzheimer’s Disease (AD): ​ ​ A neurodegenerative condition marked by progressive memory loss and language impairment. Early stages often affect the hippocampus, leading to episodic memory deficits and anomia. (part of your limbic system. This is a group of brain structures that regulate your smells, emotions, memories and autonomic behaviors (such as heart rate, breathing, sweating, etc) Agitation suggests worsening cognitive decline affecting emotional regulation. Other Neuroimaging Techniques: 1.Amyloid PET Imaging: Detects amyloid-beta plaques, a hallmark of AD. 2.Tau PET Imaging: Visualizes tau tangles in cortical areas. 3. CSF Biomarkers: Reduced amyloid-beta and increased tau levels confirm AD pathology. B) Neuropsychological Conceptualization Assessment: 1.Memory and Language: Tests: RAVLT, Boston Naming Test. Assess episodic memory and naming deficits. 2.Behavioral Symptoms: Neuropsychiatric Inventory (NPI) for agitation and emotional regulation. Rehabilitation: 1. Pharmacological Treatment: Cholinesterase inhibitors donepezil to improve acetylcholine levels. 2. Cognitive Interventions: Memory aids (e.g., digital devices, errorless learning techniques). 3. Behavioral Management: Structured routines and calming strategies for agitation. 4. Family Education: Provide caregivers with strategies to support daily activities and manage agitation. Citations: Jack, C. R., et al. (2018). “NIA-AA Research Framework: Toward a biological definition of Alzheimer’s disease.” Alzheimer’s & Dementia, 14(4), 535–562. 5 detailed differences between Conduction Aphasia, Wernicke’s aphasia, and Transcortical Aphasia: 7 1. Location of Brain Damage Conduction Aphasia: Results from damage to the arcuate fasciculus, a bundle of fibers connecting Wernicke’s and Broca’s areas, or the supramarginal gyrus in the parietal lobe. Wernicke’s Aphasia: Caused by damage to Wernicke’s area in the posterior portion of the left superior temporal gyrus. Transcortical Aphasia: Results from damage to areas outside the primary language centers (Broca’s or Wernicke’s areas) but connected to them, such as the watershed areas of the brain. Areas affected include white matter tracts deep to Broca’s area connecting it to the parietal lobe. 2. Speech Fluency Conduction Aphasia: Speech is fluent, but it may be interrupted by frequent pauses to self-correct errors. Wernicke’s Aphasia: Speech is fluent, often excessively so, but contains many semantic errors (A semantic error occurs when a word or phrase is used incorrectly in the wrong context or with the wrong meaning), neologisms (made-up words), and a lack of meaning (word salad). Transcortical Aphasia: Transcortical Motor Aphasia: Speech is non-fluent, similar to Broca’s aphasia. Transcortical Sensory Aphasia: Speech is fluent, like Wernicke’s aphasia, but with intact repetition. 3. Repetition Abilities Conduction Aphasia: Repetition is severely impaired, even for simple words or phrases, due to the disrupted connection between comprehension and production areas. Wernicke’s Aphasia: Repetition is also impaired, as comprehension of what is heard is poor. Transcortical Aphasia: Repetition is intact, often surprisingly so, even when spontaneous speech or comprehension is impaired. 4. Comprehension Conduction Aphasia: Comprehension is relatively preserved, allowing patients to understand spoken and written language well. Wernicke’s Aphasia: Comprehension is severely impaired, making it difficult for patients to understand spoken or written language. Transcortical Aphasia: Motor: Comprehension is preserved. Sensory: Comprehension is impaired, similar to Wernicke’s aphasia. 8 5. Error Patterns and Self-Monitoring Conduction Aphasia: Patients are aware of their errors and make frequent self-corrections (known as conduite d’approche), but still struggle to achieve accuracy. Wernicke’s Aphasia: Patients are often unaware of their errors and do not self-correct, leading to fluent but nonsensical speech. Transcortical Aphasia: Motor: Patients may struggle to initiate speech but are aware of their deficits. Sensory: Patients may exhibit semantic errors and poor comprehension but typically retain repetition and are often less aware of their deficits. Case 6: Traumatic Brain Injury (TBI) and Language Deficits The patient is 28 and she has suffered a TBI. Her symptoms focus mostly on language functions. Specifically, comprehension and production of speech are intact, but disturbance of repetition is the most prominent. In addition, naming and writing are also mildly impaired. In the neuroimaging, it is obvious that there are lesions between the arcuate fasciculus and the connections between Broca’s and Wernicke’s area. Other neurological symptoms of the patient include some somatosensory deficits and ideomotor apraxia A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. -->Conduction aphasia (8th, 24 slides) Conduction aphasia is a relatively rare form of fluent aphasia characterized by the inability to repeat sentences, defective use of phonemes (any of the perceptually distinct units of sound in a specified language that distinguish one word from another, for example p, b, d, and t in the English words pad, pat, bad, and bat) and impaired naming ability. By far, the most common antecedent of conduction aphasia is a cerebrovascular event (stroke). According to the classical categorization of aphasic syndromes, frontal lesions cause motor aphasias (impaired language production,) and temporal–parietal lesions produce sensory aphasias (impaired language comprehension), while lesions connecting the frontal and temporal lobes through the white matter tract known as the arcuate fasciculus cause conduction aphasia. Language production and auditory comprehension remain relatively preserved in conduction aphasia, distinguishing it from the more familiar non-fluent (Broca's) and semantic (Wernicke's) aphasias. Symptoms: Difficulty in repetition, mild naming and writing impairments. Lesions between the arcuate fasciculus and connections between Broca’s and Wernicke’s areas. Associated somatosensory deficits and ideomotor apraxia. A) Diagnosis and Neuroimaging Techniques 9 Possible Diagnosis: Conduction Aphasia: Caused by damage to the arcuate fasciculus, which disrupts the connection between Broca’s and Wernicke’s areas. Key Features: Intact comprehension and speech production. Severe impairment in repetition. Mild naming and writing deficits. Other Neuroimaging Techniques: 1.Diffusion Tensor Imaging (DTI): Visualizes damage to white matter tracts, such as the arcuate fasciculus. 2.Functional MRI (fMRI): Assesses residual activity in language networks. B) Neuropsychological Conceptualization Assessment: 1.Language Function: Boston Diagnostic Aphasia Exam/ 2. Motor and Sensory Testing: Assess somatosensory deficits and ideomotor apraxia. Rehabilitation: ​ 1.​ Speech Therapy: ​ ​ Repetition exercises and phonemic cueing. ​ ​ Writing practice to address mild deficits. ​ 2.​ Occupational Therapy: ​ ​ Focused on improving ideomotor functioning and compensatory strategies for sensory deficits. ​ 3.​ Assistive Technology: Apps for communication and writing support. Citations: Goodglass, H., & Kaplan, E. (1983). Boston Diagnostic Aphasia Examination. Case 7: Fluent Speech with Comprehension Deficits Post-TBI A patient has been referred to you, after a TBI that he suffered, from a car accident. The patient presents with fluent speech (logorrhea) but incorrect choices of sounds of words (paragrammatisms), as well as speech comprehension disturbances, and empty speech. MRI results show lesions in half of the first temporal gyrus and possible adjacent cortex too. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological Impairments. -->Wernicke’s aphasia (8th lec, 19 slide) Symptoms: Fluent but nonsensical speech (logorrhea), paragrammatisms, and comprehension disturbances. Lesions in the superior temporal gyrus. This type of aphasia doesn’t affect your intelligence. It only affects how your brain processes language. It affects your ability to make sense when speaking. It also affects your ability to understand what others are saying. Although speaking may seem easy, what you say can be confusing to others. Eg. “The green dog jump helicopter cheese on the yesterday smoodle.” 10 A) Diagnosis and Neuroimaging Techniques Possible Diagnosis: Wernicke’s Aphasia: Damage to the posterior superior temporal gyrus disrupts comprehension and meaningful speech production. Features: Fluent speech with errors (paragrammatisms). Poor comprehension and “empty speech.” Other Neuroimaging Techniques: 1.fMRI: Assesses language network activity during speech and comprehension tasks. 2.PET Scan: Evaluates hypometabolism in temporal regions. B) Neuropsychological Conceptualization Assessment: Language: Western Aphasia Battery (WAB) for fluency, comprehension, and repetition. Cognitive Screening: Tools like MMSE to check for broader cognitive impairments. Rehabilitation: ​ Speech Therapy - Semantic Feature Analysis (SFA) for improving word selection. Comprehension tasks focusing on sentence-to-meaning matching. ​ Environmental Modifications: Simplified language cues and visual aids. ​ Caregiver Training: Teach family members strategies to support communication. Citations: Kertesz, A. (2007). Western Aphasia Battery-Revised (WAB-R). Transcortical sensory aphasia (TSA) and transcortical motor aphasia (TMA) differences: 1. Transcortical Sensory Aphasia (TSA) Key Features: Fluent speech: Individuals can produce grammatically correct sentences, but the content may lack meaning (e.g., “word salad”). Impaired comprehension: Difficulty understanding spoken or written language. Intact repetition: Despite poor comprehension, they can accurately repeat words or sentences. Naming difficulty: Struggles with naming objects or finding the right words. Location of Damage: Typically occurs due to lesions in the posterior parietal or temporo-occipital regions of the brain, sparing the primary language areas (e.g., Wernicke’s area). Example: A person with TSA might hear the word “apple,” repeat it accurately, but fail to understand what an apple is or describe it. 2. Transcortical Motor Aphasia (TMA) Key Features: 11  Non-fluent speech: Speech is effortful and sparse, often limited to short phrases or single words. Intact comprehension: They understand spoken and written language relatively well. Intact repetition: Ability to repeat words or phrases remains preserved. Difficulty initiating speech: Trouble starting sentences or maintaining verbal output, though they can complete sentences with prompting. Location of Damage: Typically results from lesions in the frontal lobe near Broca’s area, often affecting the supplementary motor area or the anterior superior frontal gyrus. Example: A person with TMA might understand a question like “What is your name?” but struggle to say “My name is John,” requiring effort to begin speaking. Summary Table​ ​ ​ ​ ​ ​ ​ ​ Feature​ ​ Transcortical sensory aphasia Transcortical motor aphasia Speech Fluency Fluent but meaningless​ Non-fluent and effortful Comprehension Impaired Intact Repetition Intact Intact Naming Impaired Often intact Lesion Location Posterior Frontal lobe near Broca’s area parietal/temporo-occipital Part 2 Case 1. A 32 years old patient has been referred to you after an accident he suffered. His symptoms include spontaneous speech impairments with repetition and comprehension of speech remaining almost intact. In addition, the patient presents with telegraphic speech & lack of prosody. His MRI shows that areas affected include white matter tracts deep to Broca’s area connecting it to the parietal lobe. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. Transcortical Motor Aphasia Symptoms: Impaired spontaneous speech Intact repetition and comprehension Telegraphic speech 12 lack of prosody MRI indicates white matter damage deep to Broca’s area. A) Diagnosis and Neuroimaging Diagnosis: Transcortical Motor Aphasia (TMA) -​ TMA is caused by damage to pathways connecting Broca’s area to other brain regions (e.g., the parietal lobe), often sparing Broca’s area itself. -​ Characterized by non-fluent speech with intact repetition and comprehension. -​ Telegraphic speech and lack of prosody suggest limited syntactic production. Neuroimaging: MRI confirms white matter tract damage. Diffusion Tensor Imaging (DTI): Useful for assessing white matter integrity and connectivity. Functional MRI (fMRI): To evaluate the functionality of surrounding areas. B) Neuropsychological Conceptualization Assessment: Language Tests: Boston Diagnostic Aphasia Examination, Western Aphasia Battery. Cognitive Assessments: Attention and working memory (to ensure these are not secondary contributors). ​ ​ Motor Speech Examination: To assess for apraxia of speech. Rehabilitation Options: ​ ​ Speech Therapy: Focus on improving fluency and sentence structure using techniques like melodic intonation therapy. ​ ​ Script Training: To practice functional sentences. ​ ​ Assistive Technology: Use of communication aids if speech remains limited. Case 2. A 35 year old male patient who has suffered an injury, has been referred to you with symptoms of speech comprehension impairment (while repetition remains intact). There are also mild disturbances in meaning of the words, despite normal repetition of presented words. In his CT, damage appears in the white matter tracts connecting parietal lobe to temporal. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. (Transcortical sensory aphasia) Pay attention : Difference with Wernicke’s Aphasia include intact ability of word repetition and of no mistakes in grammar ANSWER - Transcortical Sensory Aphasia Symptoms: Impaired speech comprehension, intact repetition, disturbances in word meaning, and damage in white matter connecting parietal and temporal lobes. A) Diagnosis and Neuroimaging Diagnosis: Transcortical Sensory Aphasia (TSA) 13 ​ ​ Caused by damage in pathways linking the parietal and temporal lobes, sparing Wernicke’s area. ​ ​ Differentiated from Wernicke’s aphasia by preserved repetition ability. Neuroimaging: ​ ​ CT shows damage in relevant white matter tracts. ​ ​ PET or SPECT Scans: Useful to examine metabolic activity in affected areas. ​ ​ DTI: To assess white matter disruption. B) Neuropsychological Conceptualization Assessment: ​ ​ Comprehension Testing: Token Test, Peabody Picture Vocabulary Test. ​ ​ Semantic Processing Tests: To evaluate word meaning. ​ ​ Memory Assessment: Given possible deficits due to temporal lobe involvement. Rehabilitation Options: Semantic Therapy: Focused on word retrieval and comprehension. Auditory Comprehension Exercises: Gradual exposure to increasingly complex sentences. Contextual Learning: Use visual cues to aid understanding. Case 3. A 25 year old patient, after a vascular accident, presents with huge impairment in the fluency of speech (apraxia of speech) but no disturbance of auditory comprehension. His main symptoms include: Telegraphic speech, lack of prosody, repetition and naming impaired (agrammatism).The patient presents also motor difficulties, such as dysarthria, right hemiparesis, ideomotor apraxia. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. ANSWER Broca’s Aphasia Symptoms: Non-fluent, telegraphic speech, lack of prosody, impaired repetition and naming, agrammatism, motor difficulties like dysarthria, right hemiparesis, and ideomotor apraxia. A) Diagnosis and Neuroimaging Diagnosis: Broca’s Aphasia ​ ​ Caused by damage to Broca’s area and nearby regions. ​ ​ Associated with motor symptoms due to proximity to the motor cortex. Neuroimaging: ​ ​ MRI: Reveals infarction (mini strokes) in Broca’s area and motor cortex. ​ ​ fMRI or TMS (Transcranial Magnetic Stimulation): To assess language networks and motor connections. B) Neuropsychological Conceptualization Assessment: Language Tests: Aphasia Diagnostic Profiles (ADP). 14 Motor Assessments: Evaluate for dysarthria and apraxia. Cognitive Testing: To identify co-morbid executive function deficits. Rehabilitation Options: Speech Therapy: Emphasize structured repetition and articulation exercises. Motor Therapy: Incorporate physical therapy for hemiparesis and apraxia. AAC Devices: Alternative communication aids for severe cases. Case 4 The patient is 72 years old & presents with cognitive symptoms, such as disturbances in memory, speed of processing, visuospatial deficits, motor symptoms, hallucination, sleep disturbances & autonomic problems. In neuroimaging, the patient’s brain is present with Lewy bodies (Abnormal deposits of a protein called alpha-synuclein in the brain) and amyloid plaques, in the subcortical and cortical regions of the brain. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments. ANS - Dementia with Lewy Bodies (DLB) Symptoms: Memory loss, processing speed deficits, visuospatial impairments, motor symptoms, hallucinations, sleep disturbances, and autonomic problems. Neuroimaging reveals Lewy bodies and amyloid plaques. A) Diagnosis and Neuroimaging Diagnosis: Dementia with Lewy Bodies (DLB) Characterized by cognitive decline, fluctuating attention, visual hallucinations, Parkinsonian motor symptoms, and REM sleep disturbances. A decline in their thinking ability, especially in the areas of attention, visual perception, and executive function. Neuroimaging: SPECT or DaTscan: To evaluate dopaminergic dysfunction. Amyloid PET Scans: To differentiate DLB from Alzheimer’s disease. B) Neuropsychological Conceptualization Assessment: Cognitive Testing: Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA). Visual-Spatial Tests: Rey-Osterrieth Complex Figure Test. Behavioral Assessment: To evaluate hallucinations and fluctuations in cognition. Rehabilitation Options: Cognitive Stimulation Therapy: Focused on memory and executive function. Motor Therapy: For Parkinsonian symptoms. Sleep Management: Use of melatonin or sleep hygiene strategies. 15 Case 5 A 57 year old female patient has been referred to you with symptoms of memory impairment, disinhibition, loss of empathy (apathy), impulsivity, repetitions, social inappropriate behavior and loss of speech and motion. Her MRI scan showed large atrophy on frontal areas and restricted (so far) in temporal areas of the brain. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological Impairments ANSWER - Frontotemporal Dementia (FTD) Symptoms: Memory impairment, disinhibition, apathy, loss of empathy, impulsivity, inappropriate behavior, loss of speech/motion, and frontal/temporal lobe atrophy. A) Diagnosis and Neuroimaging Diagnosis: Fronto-Temporal Dementia (FTD) ​ ​ Behavioral variant FTD is indicated by disinhibition, apathy, and executive dysfunction. ​ ​ Progressive aphasia may also occur. Neuroimaging: ​ ​ MRI: Frontal and temporal atrophy. ​ ​ FDG-PET: To assess metabolic deficits in these areas. B) Neuropsychological Conceptualization Assessment: Executive Function Tests: Wisconsin Card Sorting Test. Language and Memory Testing: Verbal fluency and working memory assessments. Behavioral Questionnaires: For social functioning and empathy. Behavioral Interventions: Teach appropriate social behaviors. Speech Therapy: Focus on language maintenance. Cognitive-Behavioral Therapy: For managing impulsivity. Case 6 A patient has been referred to you with symptoms of impairment in speech sounds identification. Patient seems to be aware of speech but informs you that he perceives it as “foreign language” It must be taken into consideration that the patient's speech production is normal (although loud sometimes), so is the writing and reading. Neuroimaging results show bilateral temporal lesions. A) Discuss the possible diagnosis of the case (theoretical background) and suggest any other neuroimaging technique that might be helpful to the diagnosis. B) Provide a complete neuropsychological conceptualization of the case concerning neuropsychological assessment and rehabilitation options for patient's neuropsychological impairments 16 ANSWER - Verbal Auditory Agnosia Symptoms: Difficulty identifying speech sounds; perceives speech as foreign. Normal speech production, reading, and writing. Bilateral temporal lesions. A) Diagnosis and Neuroimaging Diagnosis: Verbal Auditory Agnosia (Pure Word Deafness) Damage to bilateral temporal lobes disrupts phonological processing while sparing non-verbal sounds. Speech comprehension is impaired, while other modalities are intact. Neuroimaging: MRI or CT: Confirms bilateral temporal damage. EEG or MEG: To assess auditory processing deficits. B) Neuropsychological Conceptualization Assessment: Auditory Processing Tests: Evaluate phoneme discrimination. Language Testing: Assess comprehension and lexical access. Rehabilitation Options: Auditory Training: Exercises to improve phoneme recognition. Speech-to-Text Software: To convert auditory input into text. Compensatory Strategies: Use of written instructions or visual cues. 17