An Educational Case-Report Of A Person With Vascular Dementia And Comparison With The Characteristics Of Other Dementias

Author: F Elugbadebo and A Ojagbemi

Consultant, Department of Psychiatry, College of Medicine, University of Ibadan, P.M.B 5017 (G.P.O), Ibadan, Nigeria


Akin Ojagbami, Department of Psychiatry, College of Medicine,

University of Ibadan, Ibadan, Nigeria


Phone:+44-744230 5465



The vascular dementias include a variety of severe cognitive disorders which are commonly the result of vascular risk factors, vascular disease, or both. The clinical spectrum is often varied, but may include changes in cognition, which are often severe. Additional fluctuation  in emotions and personality are also commonly seen. This case presentation attempts to describe the clinical presentation of vascular dementia, in relation to other dementias. The paper concludes that detailed personal, medical and psychiatric history, as well as clinical and neuropsychological examinations may elucidate the cognitive and non-cognitive symptoms early in the course of vascular dementia and potentially differentiate vascular dementia from other types of dementias.



The vascular dementias include a variety of severe cognitive disorders which are common, vascular dementias are the second commonest type of dementia in most clinical settings [3]. The clinical spectrum is often varied. This variation may sometimes reflect the underlying predisposing pathology. In general, the clinical picture of vascular dementia may include deterioration in memory and not less than two other domains of cognition [1]. The changes in cognition are often severe and affect the ability of the individual to function independently. Additional fluctuation in emotions and personality are commonly seen [4].

The following case description is designed to help medical students, as well as doctors in their early years of training, appreciate the unique but variable clinical presentation of vascular dementia in relation to other dementias. The case described in the following section was managed at the Old Age Psychiatry Out-patient Unit of the University College Hospital Ibadan Nigeria.

Case Presentation

Mrs M.O, a 60 year old retired nurse was referred to the Old Age Psychiatry Out-patient Unit by the endocrinologists on account of difficulty with behaviours such as undue irritability, anger outburst and hostility. She was first seen 6 years earlier and managed for type 2 diabetes mellitus, hyperlipidaemia, and systemic hypertension using relevant medications as prescribed by the endocrinologist physicians. About 2 years before the referral, she had complaints of sudden onset generalized slowness, occasional forgetfulness and unexplained weakness. The symptoms affected her ability to perform her usual chores like cooking and cleaning. In the year before her presentation to the outpatient unit, her forgetfulness was noticed to have become increasingly worse. She regularly forgot where she kept personal belongings such as her wallet and mobile phone. Repeatedly, she had to be reminded of the details of recent conversations. In addition, she was reported to have lost the ability to use money correctly over the period of her illness. As a result of this, she was stopped by her family members from shopping on her own. Eventually, she started having progressive difficulties with bathing and dressing which caused much distress to the family, especially her husband who was the principal caregiver.


The mental state examination of Mrs. M.O at presentation to the unit revealed a middle aged woman with poor attention and concentration, poor registration and immediate recall with poor short and long term memory. Her blood pressure was 130/70mmHg. The only obvious neurological examination finding was abnormal ankle jerk reflex on the left side. The results of laboratory tests for fasting glucose, fasting lipids, thyroid function tests and other relevant investigations were also within normal limits. A selection of tests from the modified version of the Consortium to establish a registry for Alzheimer ’s dis ease (CERAD) neuropsychological  battery was  administered on Mrs. M.O.  The local normative references  for  this battery had been established for the Nigerian elderly [5]. The tests revealed impairment in multiple cognitive domains. Notably, she had a score of 16 out of a minimum of 22 expected for her level of education on the mini-mental state examination (MMSE). She was able to list 6 words out of 11, after a learning phase. Furthermore, she was able to name 5 animals out of a minimum of 7. A cranial Computerized Tomography (CT) Scan showed evidence of peri-ventricular intensities that were in keeping with white matter changes. Also recorded on the CT scan were multi-focal chronic infarcts and bilateral temporal lobe atrophy.

Clinical diagnosis and treatment

On account of the overall picture, a clinical assessment of vascular dementia was made according to criteria in the fourth revision of the diagnostic and statistical manual of mental disorders (DSM IV) [6]. This was based on the following characteristics: 1), the overall profile of deteriorating cognitive impairment leading to loss in functional ability such as being unable to perform household chores, shopping, bathing and dressing without assistance; 2), the presence of vascular risk fact ors including type 2 diabetes mellitus, hyperlipidaemia, and systemic hypertension, preceding the onset of cognitive impairment; and 3), the occurrence of multiple infarcts visualized on neuro- imaging examination.

She was placed on Tabs Risperidone 0.5mg nightly because of her behavioural symptoms. In addition she was encouraged to continue with her antihypertensives, oral hypoglycaemic agents and statins which are expected to provide ongoing control over the underlying vascular risks. She was planned for follow-up review after two weeks. However, she did not return to the clinic until after 2 months. On the return visit, the husband reported some improvements, evidenced by less hostility. She stopped coming to clinic after the second consultation.


Cognitive symptoms

The patient in this case report had cognitive impairments in three broad areas: memory, attention, and executive functions. Global cognit ive impairment was psychometrically evident in her poor performance on the MMSE [5]. Specific impairment in memory was evident in her difficulties with remembering recent conversations, including the location of her personal belongings. Memory impairment was also evident in the problems she had with registration, recall, short and long term memory on the mental state examination. Psychometrically, specific problems with memory were

demonstrated by the poor performance in the word list learning test. In interpreting these changes in memory functions, it is often important to note that they may sometimes result from impairment in attention.

Impaired executive functioning may be responsible for her loss of the ability to use money correctly. This is also a reflection of impaired instrumental activities of daily living (ADL). In other perspectives, the ability to understand the correct value of money may be viewed in terms of an intact calculation ability, an aptitude that may require multiple areas of cognition such as language, memory, visuospatial abilities and executive functions [7]. Abnormality in executive functions was formally demonstrated by the poor performance in the Animal naming test. The patient in the report also had additional problems with dressing, a common problem of praxis that may also reflect impairment in self-care or basic ADL.

While most patients with vascular dementia may show variable or mild impairments in memory, these patients may exhibit more disturbances in attention and executive functions [8]. In contrast, impairment in memory functions may be a common and early presentation in Alzheimer’s disease [9]. Some patients with frontotemporal dementia, especially the behavioural variant may also show impairment in attention and executive functions that may overlap with those of vascular dementia [10]., while agnosia and severe visuo- constructional abnormalities may be more characteristic of Lewy body dementia [11].

Non-cognitive symptoms

The patient in the case report also had non-cognitive symptoms, which started with unexplained slowness and weakness, and later, irritability, anger outburst and hostility. These symptoms are referred to as the Behavioural and Psychological symptoms of dementia (BPSD). In terms of structure, the non-cognitive symptoms in the case reported may be viewed as the ‘affective syndromes’ of dementia [12]. They have also been categorised as ‘mood’ syndromes of dementia in other perspectives [13]. Yet, they have been referred to as ‘depression syndromes’ of dementia [14], or major depression [6] in other classifications. This symptom complex may be non-specific in terms of their diagnostic value in the dementias. However, as in the case report, they may be more commonly seen in the earlier or middle courses of vascular dementia [4]. Similarly, earlier presentations of ‘affective syndromes’ has been repor ted in Alzheimer ’s disea se [15 ]. Per haps, overlapping sub-cortical pathologies between, for example, depression and the sub-cortical dementias,

may explain the relatively high prevalence of the syndrome in conditions such as Parkinson’s disease dementia and progressive supranuclear palsy [16]. In contrast to the mood symptoms, the ‘behavioural’ or ‘psychotic’ syndromes of hallucinations, delusions, euphoria and disinhibition[12] may be more common in dementia with Lewy bodies and frontotemporal dementia. Visual hallucinations, in particular, may be common in dementia with Lewy bodies and Parkinson’s disease dementia [16]. The psychotic and behavioural syndromes of dementia may also sign-post progression in the severity of many types of dementia, including Alzheimer’s disease [17].


Underlying brain changes

Similar to the clinical presentation, the underlying brain changes that may be observed in vascular dementia may vary depending on the background aetiology. Vascular dementia may result from a single stroke with a strategically placed infarct. It may also take the form of multi-infarct dementia, or result from a progressive small blood vessel disease [18]. In many cases, it may occur following brain haemorrhages, or in combination with the neuro-pathology of Alzheimer’s disease [19]. Despite this varied spectrum, most cases of vascular dementia may be characterised by increased number of infarcts on CT scan images of the brain structure [20]. Many lesions may become visible in the brain white matter on Magnetic resonance imaging (MRI) scans [20]. Irregular reduction in brain perfusion may become observable in many cases of vascular dementia when brain functions are investigated using the method of single photon emission tomography (SPECT) [21]. Similarly, evidence of irregular reduction in brain metabolism may be seen on Positron emission tomography (PET) images.


Pathologically, vascular dementia may be characterised by evidence of infarcts of various sizes, as well as severe cell losses in the hippocampus, a phenomenon often referred to as hippocampal sclerosis[22]. These neuro-pathological changes in the brain of a person with vascular dementia may lead to interruptions in the neur ochemical connections between different functionally meaningful parts of the brain. In addition, the vascular events may lead to changes in the pattern of circulation and permeation of oxygen and nutrients in several brain regions [19]. Neuro-pathological changes affecting the areas around the medial temporal lobe and hippocampus, for example, may result in the impairments of memory functions [23] as seen in the case presented. Similarly, the problems with praxis may result from neuro-pathological disruptions in several temporal and parietal connections [24]. Also, there were


problems with attention and executive functions in the case report. These changes may result from abnormal neuropathology affecting the frontal lobe or its connections with, for example, the thalamus [19]. Interruptions between the pre-frontal cortex, the limbic structures, and several sub-cortical regions may underpin the affective syndromes of depression and irritability [4] as demonstrated in the case in context.


Summary, lessons and conclusion

Vascular dementia encompasses several causes of severe vascular cognitive impairments. Detailed personal, medical and psychiatric history, as well as clinical and neuropsychological examinations may elucidate the cognitive and non-cognitive symptoms early in the course of the disease. Also, such clinical assessments may potentially differentiate vascular dementia from other types of dementias. Structural and functional neuro-imaging examinations may further enhance the reliability of the diagnosis of vascular dementia. These examinations may also help specify the type and location of the vascular pathology, thus differentiating the different causes of vascular cognitive impairments. The final diagnosis of dementia may be most reliably made by the neuro-pathological examination of the brain, typically after the death of the patient.




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