Case Studies - Answers – 86 References

Answers – 86 References – 87

3.2 Case Studies

In this section we present case examples that demonstrate the role of neuroimaging in diagnostic work-up of patients in geriatric psychiatry. Because this chapter is about neuroimaging and not particular diagnostic entity, we will present one case with more clinical details, while the rest of the cases are more of a summary of clinical description and imaging findings that help highlight the value of structural and functional neuroimaging in the diagnostic process. The questions arising from the case will focus on neuroimaging mainly.

1 Megabecquerel (MBq) is a measure of radioactive material.

3.2.1

Case 1

Case 1 History

A 70-year-old right-handed retired male police officer with 14 years of education was referred to geriatric psychiatry by cognitive neurology service with a question of behavioral change in the form of “abulia” and whether this might be stemming from depression. He had relatively unevent- ful coronary bypass surgery about 5 years previously, with only subtle diplopia on left gaze since. A year before current presentation, he had pulmonary embolism and “pulmonary arrest” during a surgery to remove a benign abdominal wall tumor. Since then he has had changes in his behavior in the form of lack of interest in doing things, less talkativeness, mild disinhibition (e.g., when needing to urinate, he would do it in public places, though behind a barrier). He did have few episodes of urinary incontinence from not finding a place to urinate fast enough, which had embarrassed him somewhat, but embarrassed his family much more. His family described these changes as significant departure from his usual character; he was outgoing and conversant before the abdominal surgery a year ago. The patient had partial insight into the changes but could not explain them and did not feel bothered as much as the family by them. More recently, he slept a lot and did very little during the day, which was again very different from his usual pattern. There was no change in language, navigation, or driving skills. There were no head- aches, seizures, focal weakness, or weight loss. He tended to complete tasks that his wife left for him but would not do them spontaneously. Gait was slower with mild shuffling over the last year. Medical history was significant for diabetes mel- litus, hypertension, and sleep apnea (on CPAP machine that he used regularly), history of coronary artery bypass 5 years ago for ischemic heart disease, left eye motility limitation with diplopia on left gaze, abdominal leiomyoma, which was resected 1 year previously, and the surgery was complicated by pulmonary embolism and pulmonary arrest, as stated previously. He had no history of traumatic brain injury or diagnosed stroke and no previous psychiatric or substance misuse history. He did smoke cigarettes, 1 pack per day for 20 years, but quit about 30 years ago. He was on medications for his vascular risk factors including an angiotensin II inhibitor, a beta-blocker, and oral hypoglycemic in addition to an antidepressant (venlafaxine extended-release 75 mg daily), which was started to help with the “abulia” about 3 months previously, with minor benefit. Family history was significant for ischemic heart disease in his father and half-brother, and there was no family history of neuropsychiatric illnesses (including neurocognitive disorders).

Mental Status Examination

The patient appeared well groomed, cooperative, and alert but with a flat affect. He had sparse spontaneous speech but answered appropriately in full grammatically correct sentences.

Language assessment: Naming, comprehension, and description of picture story (cookie jar theft from Boston Diagnostic Aphasia Test [66]) were normal.

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Neurological screening: Cranial nerves were normal, and some increased tone in neck and right arm and mild cogwheel rigidity in right more than left upper limbs were noted. No bradykinesia or tremors and no other abnormal movements were present. Gait was short in strides, posture was stooped forward slightly, and there was some decrease in arm swings. Reflexes were normal and symmetrical. There were no primitive reflexes. Strength was normal; toes were downgoing on plantar reflex.

Cognitive testing: On Mini Mental State Examination (MMSE) [67], he scored 28 out of 30 (1 point lost on the 3-step command and 1 on delayed recall). On Montreal Cognitive Assessment (MoCA) scale [68], he scored 25 out of 30 (2 points lost on delayed recall (but was cued to them), 2 points on digit span, and 1 point on repetition). On paragraph recall, he recalled 17 of 21 facts immediately and 15 of 21 facts after a delay [69]. Clock drawing was normal. Semantic fluency was high (18 animal names generated per minute), while phonetic fluency (letter F) was lower but within the normal range at 12 words per minute. Trail-making Test A was performed at the 50% percentile while Trail-making Test B was at 98th percentile [70].

Mood rating: He expressed mild depressive symptoms (Geriatric Depression Scale-short version was 7 out of 15) [71].

Case 1 Questions and Answers Case 1 Questions

?Question 1. When considering the data presented from this case, what is the main differential diagnosis?

?Question 2. What is the indication of brain imaging in this case?

?Question 3. What modality of neuroimaging would be appropriate to order in this case, and why?

Case 1 Answers

Case 1 Answer 1 (Question 1—When considering the data presented from this case, what is the main differential diagnosis?)

A. Depression:

a. Primary: Typically depression would have presented earlier in life. This patient had no past history of depression, and, moreover, his current picture suggested depressive symptoms rather than full-spec- trum major depressive disorder.

b. Secondary to brain disorder: This is more likely, because depressive symptomatology is common with brain disorders due to a variety of pathologies including neurodegeneration or brain insult. (See 7Chaps.

10 and ²² for more details.)

B. Neurocognitive disorder (minor or major) due to neurodegenerative illness such as frontotemporal or Alzheimer-related neurocognitive disorder:

a. Due to Alzheimer disease: In this case we do not have clear indication of amnestic features and

cognitive screening was within normal with only minor impairment in areas of attention and memory retrieval rather than encoding, which would have been more characteristic of Alzheimer disease (see 7Chap. 18 for more details).

b. Due to frontotemporal neurocognitive disorder:

Depressive and apathy symptoms can be seen in frontotemporal neurocognitive disorder, mainly in the behavioral variant (see 7Chap. 19 for details). This is a plausible clinical diagnosis in this case and needs to be explored given the change in the patient’s social behavior relatively early in the course (manifested as disinhibition), early apathy/inertia, diminished social interest, and some neuropsychological evidence of impaired attention with relatively preserved episodic memory on cognitive screening tools [72].

C. Neurocognitive disorder due to cerebrovascular disease or other acute brain insult: This is a possible clinical diagnosis given that the onset of his illness was relatively abrupt and had been stable in course over the previous year or so since the abdominal surgery, which was complicated by the respiratory arrest. The profile of cognitive performance on cognitive screening indicates preferential impairment in frontal-executive function (as suggested by impaired digit span and repetition, better semantic compared to phonemic fluency, and by benefit from cueing on recall) and social cognition (impairment in inhibition and limited initiation) [73]. (See 7Chap. 21 for details.)

D. Normal pressure hydrocephalus: Although rare, given the changes in mental status, gait, and bladder control, one would need to rule out normal pressure hydrocephalus. This is important especially because this syndrome is potentially reversible with appropriate treatment such as cerebrospinal fluid shunting procedure [74].

E. Neurocognitive disorder due to other medical conditions: There are several possible etiologies to consider under this category:

a. The patient has a diagnosed obstructive sleep apnea.

This syndrome can be associated with significant cognitive deficits in the areas of attention/vigilance, memory, and visuospatial and executive function [75].

b. There is a host of potentially reversible conditions for neurocognitive and behavioral changes that need to be considered in this case, including brain tumors, autoimmune processes (e.g., paraneoplastic syndrome, antithyroid antibodies, systemic lupus ery- thematosus), infections (e.g., herpes simplex encephalitis), and traumatic brain injury. Although the list can be extensive, there was no indication from the patient’s history to put him at particular risk for these illnesses; however, clinicians still have to keep these conditions in the differential diagnosis when working up patients [76]. For example, illnesses like herpes simplex encephalitis can present with cognitive and behavioral changes similar to the case presented, though relatively more acute in presentation [77].

Neuroimaging in Clinical Geriatric Psychiatry

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F. Neurocognitive disorder due to substance use: This includes alcohol, anticholinergics, benzodiazepines, and other medications. Alcohol abuse needed to be explored in this case, although there was nothing in the history from patient or family report to suggest this.

Case 1 Answer 2 (Question 2—What is the indication of brain imaging in this case?)

There was a short duration of neurocognitive disorder (less than 2 years), atypical cognitive presentation (attention and executive function deficits with relatively preserved memory), unexplained neurological symptoms (left gaze diplopia, parkinsonism), gait changes, and urinary incontinence, which represented neurological signs in this patient. The 2nd and 4th Canadian Consensus Conference on Diagnosis and Treatment of Dementia recommend structural imaging when certain elements from the clinical history and exam are present including what we listed above and also cases with early-onset (younger than age 60 years), rapid unexplained cognitive decline, recent head trauma, history of cancer, unexplained neurological symptoms like new-onset severe headache or seizure, use of anticoagulants, history of bleeding disorder, and any localizing neurological signs [78].

Case 1 Answer 3 (Question 3—What modality of neuroimaging would be appropriate to order in this case, and why?)

Given that the patient had several of the criteria that sup- port ordering structural brain imaging, it is reasonable to order structural brain imaging first. The choice between CT scan and MRI scan, and between with and without contrast, is important to discuss. As discussed in the background section, CT scan is relatively easy to access and easier to tol- erate and can detect fresh blood and calcification very well, although it involves exposure to ionizing radiation, provides less detailed anatomical information, and has lower resolu- tion than MRI. Also, it is particularly less informative when it comes to posterior fossa lesions and when lesions are close to the bony structures. For the patient in this case, the clinical process was no longer acute, and there were no major neurological signs, but there was a history of respiratory arrest with the possibility of anoxic/hypovolemic injury, which is usually difficult to detect with CT when is not in the acute phase. Also, an MRI can give more anatomical details and can detect smaller lesions in strategic locations. Although there was nothing in the history to suggest this, tumors are to be ruled out and the use of contrast is usually reserved to cases which metastasize.

Case 1 (Continued)

After basic screen with blood work and confirming that there was no other systemic medical, psychiatric, or substance- related disorder that could have contributed to the case, a brain MRI was ordered to rule out normal pressure hydrocephalus, cerebrovascular accident, and any other incidental finding related to traumatic brain injury, inflammation, and tumors and to evaluate regional brain volumes.

Radiology report: A multiplanar, multisequence MRI of the brain was performed without contrast. There was a finding of mild global cerebral atrophy without any regional specificity. Ventricles were within normal limits, although there was a mild right lateral anterior periventricular edema- tous signal change that could represent transependymal cerebrospinal fluid flow. No mass or midline shift was seen. A finding of symmetric high signal on T2 sequence at the junc- tion of the internal capsules and lentiform nuclei bilaterally could represent lacunar infarctions. Otherwise, there was no evidence of acute stroke or acute or chronic hemorrhage.

Few white matter hyperintensities were distributed bilaterally that may indicate microangiopathic lesions. Hippocampi were symmetrical with no particular atrophy or abnormal signal intensity.

.Figure 3.4 shows selected images form the clinical T2 MRI obtained without contrast. They show evidence of lesions bilaterally involving the basal ganglia in the proximity of the globus pallidus. This area is part of the default mode network and is strategic in attention and mood regulation.

Additionally, this area is considered “watershed” in terms of blood supply and is vulnerable for hypoxic-hypovolemic injury. This patient sustained a respiratory arrest during his surgery a year previously, which likely resulted in these lesions. The lesions are strategic for cognitive and emotional processing and could potentially explain his presentation.

The final diagnostic impression was mood and personality changes due to cerebrovascular changes. These lesions could also explain the subtle changes in his gait. Because of an abnormal signal adjacent to the lateral ventricles, suspicion of increased cerebrospinal fluid pressure was reported and a flow study was suggested. A flow study was performed under fluoroscopy with radioactive material injected to the cerebrospinal fluid. The study was reported negative for normal pressure hydrocephalus.

With the addition of the antidepressant bupropion (through enhanced dopaminergic transmission) to the venlafaxine in his medication regimen, his apathy had improved, and his gait became faster, but, unfortunately, he suffered two non-injurious falls mainly due to being faster while still having problem with gait apraxia. His bupropion was tapered and discontinued and he continued with venlafaxine XR 75 mg daily, later increased it to 225 mg daily; however, this increased dose did not improve clinical response and was confounded by worsening of his constipation. The option of adding an acetylcholinesterase inhibitor was considered, given the evidence in gait modulation [79], but this was thought to be still speculative and off-label and not sup- ported by current clinical guidelines for the treatment of vascular neurocognitive impairment [78].

Case 1 Analysis The patient had a mild neurocognitive disorder due to cerebrovascular accident. He had prominent apathy rather than depression, because he was showing limited moti- vation and initiation from lack of concern rather than negative emotional experience. He suffered mild apraxia of his gait due to frontal-subcortical disconnect.

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3.2.2

Functional Imaging Brief Cases

Case 1

A 47-year-old female with cognitive symptoms, on examination showing decreased encoding and executive function deficits. Her cognitive scores were MMSE 29 and MoCA 28.

She reported being diagnosed with fibromyalgia, but otherwise had no other pertinent medical history. Members of her family had been diagnosed with Alzheimer disease (mother and two maternal aunts), all after the age of 70. She had recently undergone an MRI study, which was reported as normal. An ¹⁸F-FDG PET scan was performed per protocol described above. Please see .Fig. 3.5.

Interpretation: This was a normal study. There was no significant left/right asymmetry, the ratio of activity of the cerebral cortex to that of the cerebellar cortex was clearly above 1 (more about this later in the chapter), and the activity of polymodal associative regions was higher than that of primary motor and somatic (but not visual) cortices. The posterior portions of the cingulate gyri showed uptake higher than that of other cortical areas (more about this later), again with the exception of the primary visual cortex (calcarine cortex).

Activity of the mesial temporal structures and of the insular regions was normal. Uptake in the basal ganglia, thalamus, and cerebellum was symmetrical. The brain stem was unre- markable.

Although the goal is not to instruct how to read such studies, the above description merely aims to draw attention to the type of interpretation, which should be performed. In the present clinical context, a normal result had significant prognostic implications, indicating a low (< 10%) risk of ongoing cognitive deterioration linked to a neurodegenerative process over the next 3–5 years [80].

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