It is believed that various regions of the Medial Temporal Lobe (MTL) are majorly involved for the coordination activations in disparate parts of the cortex, and these activations help in the information representation for the Autobiographic Memories (AM). Hence, any type of physical damage to the MTL would cause difficulty in the retrieval of AM.
Patient M.S. suffered from long-term visual memory loss along with some semantic deficits, he also exhibited severe retrograde (inability of retrieving previous memories) amnesia and moderate anterograde amnesia (inability of making future memories). Also, one unusual thing about this case was that the type of amnesia from which M.S. was suffering wasn’t similar to any of the known types of amnesia, i.e. typical medial-temporal or lateral-temporal amnesia, rather it is strongly suggested that his visual deficits contributed majorly to his autobiographic amnesia.
Also, I’ve attempted to explain the case of M.S. by using the integrated memory model by Baddely (1974).
Now, here our main focus would be to study in detail the case of M.S., one of the 11 patients who were previously identified as having VMDA (visual memory deficit amnesia). As I’ve mentioned earlier, this type of amnesia is different from the normal types of amnesia. First of all, multiple attempts were made to determine the type of amnesia he was suffering from and to prove the consistency of visual deficits with VMDA, thereby examining the role of visual imagery and visual regions in AM (autobiographic memory).
The MTL and diencephalon coordinate to activate various parts of the cortex which help to recollect information about a particular memory. MTL trauma tends to cause profound, ungraded anterograde amnesia (AA). Retrograde amnesia (RA) is often temporally graded; older retrograde memories are more likely to be spared than newer retrograde memories (Squire,1992).
Farah in 1984 suggested that patients with particular visual imagery impairment, specifically an impairment of long-term visual memory, would meet any of the following three criteria. First, the patient would be able to copy line drawings, thereby showing that other deficits are not caused by basic perceptual problems. Second, the patient would be unable to recognize objects by sight, defined as an inability to indicate either their names or their functions. Third, the patient would be unable to draw objects from memory, describe their visual properties from memory, or detect a visual image of them upon introspection. The first two criteria identify the patient as an associative visual agnostic; the third criterion demonstrates that the deficit arises from impaired access to long-term visual memory rather than difficulty generating or manipulating images. Patients who meet the third criterion but not the first two—those who cannot draw from memory but are not agnostic—have intact recognition memory for visual stimuli. Thus, patients only have a long-term memory deficit if they meet all three criteria.
Let us now discuss the details of the case study, but first, let us go through a small character sketch of the patient M.S. was tested regularly since 1971. He is a left-handed Caucasian male with no family history of sinistrality. In 1970, while a 23-year-old police cadet, he suffered a febrile illness with frontal headache and vomiting. He was diagnosed with probable herpes encephalitis; antibody tests were negative, but MRIs taken in 1989 are inconsistent with a vascular etiology. M.S. now presents with left homonymous hemianopia, but his visual acuity is normal (6/6, N5 for near vision). He also has achromatopsia, associative visual amnesia, and amnesia. His linguistic skills are generally excellent, and he has no significant aphasic symptoms; he reads a newspaper and often completes the crossword. M.S. used to tell the same stories repeatedly, probably because he used to forget the fact that he has already told them before.
Now, I’ll like to discuss the various tests that were performed on the patient M.S. and whose conclusions were then summed up:-
- A neuroimaging test was conducted in which MRI reports showed several damages on the temporal lobe and the occipital lobe of the patient. In the left temporal lobe, the temporal pole, parahippocampal gyrus, hippocampus, amygdala, and 4th temporal gyrus were destroyed; the 1st, 2nd, and 3rd temporal gyri were generally spared. Whereas, the right temporal lobe was largely destroyed along with the occipitotemporal junction.
- Visual imagery test was conducted in which M.S. was told to copy the drawing of a rhinoceros. M.S worked clockwise from the ear and used a line-by-line technique of copying. M.S scored a 75% on the copy, 13% on immediate recall, and 0% on delayed recall.
- Object recognition ability was also tested by showing several items to M.S. He wasn’t even able to recognize his own drawing of a rhinoceros and thought of it to be that of a dog. When presented with a data set of drawings and items, he recognized 0/30 fruits and vegetables, 0/30 animals, 16/30 household objects, 18/36 living items, and 28/36 non-living items. M.S. also had difficulty with face-recognition tasks. In previous tests, he had scored 33/55 on the Benton Test, 13/24 with changed orientation, and 15/24 with changed lighting, while controls scored 74.4/80.
- It was suspected that M.S. might be having semantic deficits in addition to his visual memory deficits. So in some prior testing, he could recognize only 20/36 objects from verbal descriptions of their functions (Newcombe et al., 1989). When asked to generate exemplars for living and non-living categories, he performs well below normal for living items but is at normal levels for non-living items (Young et al., 1989). He is unable to define some words (e.g. “nightingale”; Ratcliff and Newcombe, 1982).
- An Autobiographical Memory Interview of M.S. was taken in which he was interrogated about some events from his past. M.S. was almost normal for the personal semantic components but he was way below normal in autobiographical portions of his past life.
Now, let us use one of the three memory models discussed in the class to approximately explain the above case. In my opinion, the Integrated Memory Model best explains this case, a memory model given by Alan Baddeley and Hitch in 1974.
We can undoubtedly conclude that the perception of M.S. was absolutely fine (by his visual imagery test, point no. 2), but he wasn’t able to recall things properly, even when questioned immediately. According to the above memory model, visual information is fetched to the episodic buffer via the visuospatial sketchpad, and it is this process that is getting obstructed.
Working memory tasks with visual objects have activations taking place mostly in the left hemisphere, whereas tasks with spatial information activate more areas in the right hemisphere.
The visuospatial sketchpad is one of the major components of the working memory model.
We can easily see from the above flow chart that there must be some kind of obstruction in the information processing from the episodic buffer to the long-term memory which accounts for the struggle experienced by M.S. while recalling his own rhinoceros drawing, instead thinking of it as that of a dog.
M.S. almost failed the object recognition tests, in which he was supposed to recognize some commonly used objects in routine life, indicating that the semantic portion of his brain was damaged by the trauma. The episodic buffer is assumed by Baddeley to have long links to long-term memory and semantic meaning, which is clearly affected here.
Also, it goes without saying now that his autobiographical memory component was deeply affected (Conclusion from the AM Interview). The integrated working memory model displays how the modularity of the brain both at the perception level and at the retrieval, it also clearly explains how damages to these areas will affect the processes involved with the same.
Criticism of the Integrated memory model
I’ve earlier mentioned in the text that is model is only an approximation and there are some aspects where this model might not that accurately explain the above case. Like using the episodic buffer theory to explain the semantic deficit wasn’t that good, instead, I would like to use the levels of processing model as it says that retaining facts (semantics) is much easier when the brain has some visual info as the background.
Also, how the central executive memory exactly works is still left to be deciphered as there isn’t any proper experimental evidence for it.
M.S could reproduce some of the drawings on immediate recall and none on delayed recall.
This effect wasn’t explained properly by the working model memory as it is implicitly assumed in this model that the processing ability of an individual is invariant of time, which isn’t the case practically.
So from the above case study, we can conclude that the patient M.S. was suffering from a very peculiar case of visual memory loss and autobiographical amnesia, a not-so-common type of amnesia. We’ve above attempted to explain this case using the Working Memory Model by Baddeley and Hitch. Also, a brief discussion is considered over the aspects where this model fails to explain the case properly. There is one very important learning from this case that people who suffer from strokes have a chance of developing cognitive deficits that result in anterograde amnesia, since strokes can involve the temporal lobe in the temporal cortex, and the temporal cortex houses the hippocampus. Discussing the criticism of the model used also conveys us an important fact about psychology no model of memory is perfect, there are failures in almost every model of memory, and our aim is to just minimize them!
In the end, we shall appreciate the patience and efforts made by patient M.S. during the course of the whole research, despite the fact that he would have forgotten his contributions!