Well I’ve been sat here for around 10 minutes looking at this blank whiteness of the page and being totally unable to recall anything about the thing that I was about to write about.

Nothing, it’s just gone. Replaced by a blank empty nothing. Absolutely nothing, I can’t even think of a thing. Grrrr it’s so frustrating on so many levels. I do try and just laugh because there isn’t anything I can do about it.

So, this week I got the results of the brain scan. Good news and bad news.
The good news is no mass in there, no brain tumour which was a huge relief.

The bad news is that there is much active damage been done and is still actively being done in my frontal lobe.

The answer to minimise the damage is steroids, prednisolone. It looks like intravenous steroids is the only course to help me.

I’m not having it, there is no way on planet earth I am having this treatment again. Last time I had it it laid me flat on my back for over 6 months. All my illnesses put together are nowhere near as bad as the side effects from this drug. I literally spent 6 months on the couch being sick, the sickness never went away even for one minute. It was horrific. Everyone around me thought I was dying.

The difference between then and now is I had a husband back then, my daughters Father and he put aside his business to look after me. Now I have no one to look after me and even if I did, knowing what I know now I wouldn’t put another person through it.

So, I just pray this attack is nearing the end now and that the damage done will in some small way heal even if only slightly. My brain is full of scars but never before has it hit my frontal lobe, the place that controls your personality. That is the one thing I don’t want to alter because despite my quirky odd eccentric ways, I actually really like me just the way I am lol.

I just came across the name of the man who discovered multiple sclerosis, his name is Charcot. Well Mr Charcot I have had double helpings of you because I also have the muscle wasting condition called Charcot-Marie-Tooth disease (it’s nothing to do with your teeth lol)

But I’m grateful he discovered these illnesses and all the research that has gone into them. People who know me know how I feel about taking prescription drugs, as a rule I just won’t, apart from my heart medication.

I have no idea what I am waffling on about so I’ll leave it there and copy and paste some info for fellow MS sisters and brothers who may also one day be struck in the frontal lobe.

On a happier note I am meeting up with my daughter today and we’re going out for a meal later. So I’m very grateful for that and now I’ve gone blank again grrrr. Sorry folks.

I hope everyone has a lovely day.

God Bless, Su x

I guess I have a lot to read up on and take in.

Historical note and nomenclature
Jean-Martin Charcot, the 19th-century neurologist who named multiple sclerosis, described prominent cognitive and neuropsychiatric symptoms in this disease (Charcot 1877). Subsequent early 20th-century writers on multiple sclerosis ignored the cognitive changes but emphasized the presence of euphoria. As neurologists stressed the white matter nature of multiple sclerosis, they further downplayed any cognitive or other “gray matter problems.” They explained depression among multiple sclerosis patients as a logical reaction to physical disabilities. In recent years, investigators have rediscovered that cognitive impairment and biological depression are significant manifestations of multiple sclerosis (Siegert 2005; Lebrun and Cohen 2009).

Key points
• Both cognitive disturbances and neuropsychiatric disorders can be observed in multiple sclerosis.
• Mild cognitive disturbances are common among patients with multiple sclerosis and are sometimes observed within the early stage of the disease.
• Memory problems are the most common cognitive deficits.
• Neuropsychiatric symptoms include depressive symptoms, agitation, anxiety, irritability, apathy, euphoria, disinhibition, hallucinations, aberrant motor behavior, delusions, sleep disorders, and sexual dysfunction.

Historical note and nomenclature
Jean-Martin Charcot, the 19th-century neurologist who named multiple sclerosis, described prominent cognitive and neuropsychiatric symptoms in this disease (Charcot 1877). Subsequent early 20th-century writers on multiple sclerosis ignored the cognitive changes but emphasized the presence of euphoria. As neurologists stressed the white matter nature of multiple sclerosis, they further downplayed any cognitive or other “gray matter problems.” They explained depression among multiple sclerosis patients as a logical reaction to physical disabilities. In recent years, investigators have rediscovered that cognitive impairment and biological depression are significant manifestations of multiple sclerosis (Siegert 2005; Lebrun and Cohen 2009).

Clinical manifestations
The neurobehavioral aspects of multiple sclerosis include both cognitive disturbances and neuropsychiatric disorders. Cognitive difficulties in multiple sclerosis involve memory retrieval, mental processing speed, reasoning and goal-oriented behavior, verbal fluency, and visuospatial skills (Rao 1990; Beatty 1993; Brassington and Marsh 1998; DeSousa et al 2002). Neuropsychiatric disturbances are primarily mood disorders (Minden and Schiffer 1990). In a meta-analytic analysis including 57 studies with 3891 participants with relapsing-remitting multiple sclerosis, it was found that larger effects were observed in cognitive domains of motor functioning, mood status, and memory and learning (Prakash et al 2008). In general, however, cognitive impairments are more severe and extended in primary progressive than in relapsing-remitting multiple sclerosis (Ruet et al 2013). Similar to other neurologic symptoms, the neurobehavioral aspects of multiple sclerosis may be present in either relapsing attacks or in a chronic progressive course, although the cognitive profiles may be partially different (Rodrigues et al 2011).
Mild cognitive disturbances are common among patients with multiple sclerosis and sometimes are observed within the early stage of the disease (Faiss 2007). Forty-five percent to 65% of multiple sclerosis patients have deficits on neuropsychological testing (Rao 1995; 1996; Brassington and Marsh 1998; Bagert et al 2002). These cognitive deficits are not usually as severe as in comparably disabled patients with Alzheimer disease or other dementias. Moreover, many cognitively impaired multiple sclerosis patients either do not complain of cognitive difficulties or complain of nonspecific forgetfulness or mental fatigue (Mendez 1995), even though significant cognitive impairment may already exist at the onset of multiple sclerosis (Achiron and Barak 2003). Frequently, general intelligence, language, and certain aspects of primary and implicit memory are preserved (Rao 1995). Although multiple sclerosis patients have an increased difference in verbal-performance IQs of 9 to 15 points, this difference results in part from sensorimotor deficits on timed subtests (Rao 1990). Nevertheless, individual multiple sclerosis patients may become severely demented or markedly impaired from cognitive deficits such as frontal-executive disturbances (Beatty 1993). Amato and colleagues followed 45 multiple sclerosis patients for 10 years (Amato et al 2001). Only 20 of 37 patients who were cognitively unimpaired on initial testing remained so by the end of this time period (when the proportion of subjects who were cognitively impaired reached 56%). Degree of physical disability, progressive disease course, and increasing age predicted the extent of cognitive decline. Severity of cognitive impairment significantly correlates with physical disability (Lynch et al 2005) and with depression severity (Arnett 2005). It has been suggested that slowed information processing speed and, secondarily, deficient nonspeeded central executive skill may be core to the cognitive deficits characteristic of depressed multiple sclerosis patients (Arnett et al 1999). Interestingly, males are especially vulnerable to cognitive deficits (Beatty and Aupperle 2002; Schoonheim et al 2012) and also present more extensive white matter abnormalities (Schoonheim et al 2013). Cognitive impairments are also observed in children with multiple sclerosis (Bigi and Banwell 2012). Childhood and juvenile cases are associated with low IQ scores and general cognitive impairments (Amato et al 2008). Those with longer disease duration and younger age of onset are at greatest risk (Banwell and Anderson 2005). The name “multiple disconnection syndrome” has been proposed for referring to the diversity of neuropsychological deficits observed in multiple sclerosis (Calabrese 2006).
Memory problems are the most common cognitive deficits in multiple sclerosis (Tsolaki et al 1994; Daly et al 2001). Furthermore, beginning during the early stages of the disease, memory impairments may be prominent (Zarei et al 2003). In a sample of 100 patients, it was observed that 71% had memory impairment; among the affected individuals, 35% of patients had mild to moderate, 19% had moderate to severe, and 17% had severe memory defects (Sedighi 2011). The main memory problem is deficient retrieval from secondary (recent and remote) memory of both verbal and visual information (Beatty et al 1988; Grafman et al 1990). Deficient retrieval is consistent with recall difficulty in the presence of near normal recognition memory (Grafman et al 1990). Disturbed retrieval also affects recent memory tasks, such as the ability to recall words from the beginning of a supraspan list (primacy effect). Disturbed retrieval also affects remote memory tasks, such as recalling famous faces from different decades or remembering autobiographical information (Beatty et al 1988; Grafman et al 1990; Paul et al 1997; Kenealy 2000). In contrast to secondary memory, primary memory, which is responsible for immediate recall, is generally intact. There is a normal digit span, a normal recency effect on supraspan recall, and normal primary memory decay on the Brown-Peterson Test (Grafman et al 1990). Multiple sclerosis patients perform comparable to normals on implicit memory tasks such as motor skill acquisition and priming (Grafman et al 1990; Beatty 1993). Gaudino and colleagues observed that the primary problem in multiple sclerosis with regard to memory functioning is in the acquisition of new information (Gaudino et al 2001). It has been suggested that automatic memory processing is intact in multiple sclerosis, but impairment in memory, in metamemory, and in other cognitive tasks becomes evident over time when patients rely on conscious processes (Scarrabelotti and Carroll 1999).
In addition to memory difficulty, multiple sclerosis patients may have other cognitive deficits. First, information processing speed decreases, evidenced by psychomotor retardation, slowed complex reaction times, rapid fatigue, and disturbed rates of mental processing on neuropsychological measures (Piras et al 2003; Schwid et al 2003; Bodling et al 2012); the degree of fatigue is related to processing speed impairment (Andreasen et al 2010). Cognitive slowing has been observed to be significantly associated with brain volume loss (Lazeron et al 2006) and global gray matter atrophy (Morgen et al 2007; Rudick et al 2009; Llufriu et al 2013). Widespread slowing of automatic and controlled information processing underlies much of the cognitive difficulty of patients with multiple sclerosis (Kujala et al 1994). Multiple sclerosis individuals show declines in cognitive performance during a single testing session and fail to show the improvement typically seen in healthy control subjects (Krupp and Elkins 2000). De Sonneville and colleagues investigated focused, divided, and sustained attention as well as executive function and attempted to pinpoint deficits in attention control to peripheral or central processing stages (De Sonneville et al 2002). The results substantiate the hypothesis that the slowing of attention-demanding (controlled) information processing underlying more complex cognitive skills is general (ie, irrespective of type of controlled processing), with multiple sclerosis patients being 40% slower than controls. Seemingly, neural networks involved in processing speed differ between multiple sclerosis and normal subjects (Genova et al 2009). Multiple sclerosis patients may suffer from focused, divided, and sustained attention deficits as well as compromised central processing stages. Secondary progressive patients show the most extensive range of deficits, closely followed by primary progressive patients; relapsing-remitting patients appear to be much less affected. Working memory deficits have also appeared in multiple sclerosis, further contributing to cognitive deficits (Sfagos et al 2003).
There are frontal-executive problems in concept formation, abstract reasoning, planning, and organization. Disturbances in information processing speed, attention control (Whelan et al 2010), and cognitive-motor dual task performance (such as walking and performing a cognitive task) (Hamilton et al 2009) have been documented. These problems are inferred not only from behavioral observations, but also, indirectly, from change-of-set tasks such as the Wisconsin Card Sorting Test, Categories Test, and others (Rao 1990; Macniven et al 2008). Chronic progressive patients particularly may exhibit decreased executive functions and poor planning, as demonstrated on the Towers of Hanoi Test (Arnett et al 1997). Further, multiple sclerosis patients also have impaired ability to generate and apply working strategies when performing novel tasks (Birnboim and Miller 2004). Third, there is a decline in verbal fluency or word-list generation and a milder decrease in confrontational naming. Other language skills are relatively preserved, and aphasias are rare. Finally, multiple sclerosis patients may be unable to copy a complex figure such as the Rey-Osterrieth figure or perform on measures of egocentric orientation such as Money’s Road Map Test (Beatty et al 1988). Some deficits in visual and spatial processing have also been reported (Laatu 2001), including spatial neglect (Gilad et al 2006). These changes may result from decreased planning and organization rather than from primary visuospatial deficits. Benedict and colleagues studied the association between regional measures of cortical atrophy and neuropsychological dysfunction in 35 multiple sclerosis patients (Benedict et al 2002a). The authors concluded that cerebral atrophy predicts neuropsychological impairments. Regions of cortex most susceptible to atrophic and cognitive changes in multiple sclerosis are the right and left superior frontal lobes. Other authors have also found that frontal atrophy is significantly associated with neuropsychological measures of executive functioning (Locatelli et al 2004).
Cognitive defects are less prominent in individuals with greater lifetime intellectual enrichment, suggesting that intellectual enrichment represents a protective factor (so-called “cognitive reserve”) against disease-related cognitive impairments in multiple sclerosis (Sumowski et al 2009; 2010). Different authors have emphasized the protective effect of cognitive reserve in multiple sclerosis cognitive dysfunction (Feinstein et al 2013; Sumowski and Leavitt 2013). However, cognitive reserve protection may become ineffective with progression of damage (Amato et al 2013).
A specific pattern of cognitive decline has been proposed. The first cognitive difficulty refers to a general slowness that affects motor execution and cognitive processing (Olivares et al 2005). Verbal fluency and verbal memory appear to be affected early in multiple sclerosis. The pattern of cognitive decline is further characterized by a decrease in visuospatial learning, followed by delayed recall, and then by attention and information processing speed (Achiron et al 2005). Cognitive decline over time is most likely to be found in those complex tasks simultaneously requiring multiple abilities (Huijbregts et al 2006). In an 8-year longitudinal study in 31 patients, Bergendal and colleagues found a pronounced decline in speed of information processing, finger-motor speed, copying geometrical designs, episodic memory, and visuospatial short-term memory (Bergendal et al 2007). In contrast, there was no evident time-related decline in verbal abilities. A 10-year follow-up of a population-based study in Stockholm including 166 patients analyzed walking ability, manual dexterity, cognitive function, mood, activities of daily living, and social/lifestyle activities (Chruzander et al 2013). The proportion of participants who had disability in cognition, mood, and social/lifestyle activities remained stable, whereas the proportion with disability in walking, manual dexterity, and activities of daily living increased. Disease severity was significantly associated with all studied variables of disability. Older age and depression were correlated with mortality.
It is assumed that some factors can predict the cognitive evolution. In a 40-patient sample recently diagnosed with multiple sclerosis and followed up at 1, 2, 5, and 7 years, Deloire and colleagues found that the main predictors of cognitive changes over 7 years are baseline diffuse brain damage and progressive central brain atrophy over the 2 years after multiple sclerosis diagnosis (Deloire et al 2011).
Neuropsychiatric symptoms are common in multiple sclerosis (Feinstein 2004). In 1 study of 44 multiple sclerosis patients, a neuropsychiatric inventory revealed symptoms in 95% of these patients including depressive symptoms (79%), agitation (40%), anxiety (37%), irritability (35%), apathy (20%), euphoria (13%), disinhibition (13%), hallucinations (10%), aberrant motor behavior (9%), and delusions (7%) (Diaz-Olavarrieta et al 1999). Sleep disorders (Fleming and Pollak 2005) and high levels of sexual dysfunction (Schmidt et al 2005) are also frequently observed in patients with multiple sclerosis. It has been observed that personality disorders correlate with cognitive impairment (Benedict et al 2001). By the same token, some association between cognitive decline and depressive symptoms has been observed (Barwick and Arnett 2011).
Mood disorders occur more frequently in multiple sclerosis than in other chronic disabilities. Depression may present as an early sign in multiple sclerosis and may be followed by cognitive impairment (in particular, deficits in visuospatial short-term memory) before physical disability appears (Haase et al 2003). Taken together, major depression, bipolar illness, and dysphoria occur in 37% to 54% of patients with multiple sclerosis (Minden and Schiffer 1990; Diaz-Olavarrieta et al 1999). Surridge, in his original landmark study, found depression in 27% of 108 multiple sclerosis patients versus 13% for muscular dystrophy controls (Surridge 1969). Whitlock and Siskind found depressive symptoms on a depression inventory among 14 of 30 multiple sclerosis patients versus 10% of a control group with mixed neurologic diseases (Whitlock and Siskind 1980). Psychological reactions to the disabilities of multiple sclerosis can lead to further depression, anxiety, a feeling of helplessness, loss of control, and self-blame. In addition, one should separate depression from the frequent presence among multiple sclerosis patients of pseudobulbar affect with emotional incontinence (Feinstein et al 1997).
Multiple sclerosis patients have a high incidence of manic episodes (Heila et al 1995; Hurley et al 1999), panic attacks (Andreatini et al 1994), and obsessive-compulsive symptoms (Miguel et al 1995). Furthermore, a schizophreniform psychosis may occur in multiple sclerosis patients, but this association is rare (Carson and Searle-White 1996).
The neurobehavioral aspects of multiple sclerosis are related poorly to most other aspects of this disease. Although the first episodes of major depression frequently occur during periods of exacerbation of multiple sclerosis (Scott et al 1996), most cognitive and mood changes do not correlate with other neurologic findings or disability measures (Rabins et al 1986; Beatty et al 1990). One exception is an association of severe cognitive impairment with frontal gait apraxia and frontal release signs in the lower extremities (placing and grasping with the feet) (Franklin et al 1990; Mendez and Frey 1992). Another exception is the association of euphoria and eutonia with significant cognitive impairments, more extensive neurologic disability, and advanced demyelination (Rabins 1990). Second, there is a weak relationship among cognitive deficits, euphoria, eutonia, and the severity and duration of multiple sclerosis (Rabins 1990). In fact, neurobehavioral changes can occur early with minimal physical changes, and multiple sclerosis may present as a rare isolated dementia (Mendez and Frey 1992; Hotopf et al 1994). Third, studies indicate that patients with a chronic progressive course are more likely to experience memory difficulties, frontal-executive disturbances, euphoria, and eutonia (Franklin et al 1988; Rabins 1990).